So welcome to the Multi-Institutional Sports Medicine Conference. As we, it's three o'clock and over a hundred people already signed up, so thank you all very much. For all of you, again, try please to keep your microphones muted, though I think we've been able to figure out how to do that from here. Again, this is being recorded. It'll be on the transfer to the OSSM Learning Management System and available the week after. So tomorrow we should be downloading everything to the OSSM, and so for next week they should have this week's talks all set up for us. After Dr. Feeley's talk, you can submit questions on the chat and we'll answer it at the end. We'll also, if there's some faculty that want to participate, chime in, contribute, give comments. Also, just let me know and I'll try to unmute you. Hope I can see it. My layout today is a little bit different, but without further ado, we're very fortunate to have Brian Feeley, Professor of Orthopedic Surgery in residence, I think, no less, at UCSF. And he's going to be talking about the role of muscle atrophy in rotator cuffs. So without further ado, Brian, thanks so much for being here with us. No problem. Let me see if I can figure out how to do this. Um, can you guys hear me okay? Somebody? Anybody? Yeah, I hear you fine. Awesome. Okay, so I'm going to try to talk for about 25-30 minutes about rotator cuff muscle quality and outcomes. I really appreciate what Dr. Safran and everybody has set up. And in looking at this, this is really kind of a unparalleled opportunity for you all to learn from a group of experts and the rest of us who are just kind of following along. So thank everybody else who's done this. One of the things I wanted to start with is just some of the things that I've really enjoyed about the last month. And clearly, I enjoy wearing t-shirts to work. I think this is something that I'm looking for a national change that we go polo shirts or t-shirts only. We do have extra time to do some activities. Early on, I thought it was amazing to get a bunch of papers done. Our fellows are pretty much done writing. That kind of has morphed into having more time with the family and making the teenagers actually communicate with us has been pretty great. The thing I realized that I think is the hardest for a lot of us is seeing the inside of my patients' houses. I never knew that my patients were essentially cat people all set up. But now that I've seen most of the most of the Bay Area's inside and most of the people in Fresno, I feel like almost everybody has five or more cats. So it's definitely a different perspective in terms of practice management and learning more about your patients in ways that I never thought I'd actually have to do. What I want to convince you of after today is that our classification systems for muscle quality aren't all that reliable and we may need to move away from using these. That quantitative imaging is probably the next step forward. And for those of you that are familiar with our program, you know that we have a strong MRI quantitative imaging group, both for me and shoulder outcomes. You've probably already been taught this, but we'll go into a little bit more depth about why muscle quality is an important predictor of rotator cuff status. How atrophy and fatty infiltration, which I do believe are separate but related processes, don't improve after repair, no matter how many rows you put in. And I wanted to talk a little tiny bit about basic science and then we'll do some case presentations. So just to get you all thinking, this is a 57 year old male with five months of right shoulder pain. He's right hand dominant, tried a home exercise program, didn't really help that much. He takes NSAIDs when he remembers, makes his shoulder feel better. But he says he continues to have pain at night and pain with overhead activities and he used to play tennis two or three times a week and now he's kind of stopped doing that and he's gone to just kind of running and a lower demand type exercise program. So when he comes in and sees you, he's got full range of motion. He's got some subjective weakness and he's got some impingement signs. Nothing's horrible. X-rays are normal and thankfully he comes in with an MRI and it shows a small to medium sized rotator cuff tear. Doesn't seem to really involve the anterior cable, but he's got some mild fatty infiltration and then a little bit of atrophy. So as we go through this, I want you to think about how you would manage this patient, which I think is a pretty consistent and common patient that we see. Now, when we talk about muscle degeneration, we tend to group fatty infiltration and atrophy into one bucket. We tend to call it fatty degeneration, fatty atrophy, or just muscle degeneration. However, moving forward, I want you to think about these as two distinct processes, both when you're thinking biologically about how they may happen and when you're thinking about MRI reading for classifications. And one of the things I think we find most commonly is our residents and fellows, when we ask them to quantify fatty infiltration, they often just look at based on muscle size, which is not entirely accurate. Now, the classification systems that you need to know as fellows and any senior residents that are present, the most important one that we tend to ask about is the Goutelier classification. So the Goutelier classification is a classification where there is an entirely qualitative system. It's no fat, streaks, muscle more than fat, fat more than muscle, and almost entirely fat. And even when I look at this, which is the classic picture of Goutelier, I would argue that B and C don't actually look that much different, and D and C don't look all that much different. Sorry, my computer froze for a sec here. We don't talk about classifying atrophy nearly as much, but the most common system was described by Dr. Warner. It's also a qualitative grading system with none, mild, moderate, and severe based on the tangent along your scapular Y. When we look at classification systems for cuff tear arthropathy, there's two, the Hamada system, which is shown here, which is grade one, which is essentially mild superior subluxation, grade two, considerable subluxation, grade three with some changes on the under surface of the acromion, and then for A and B when you're starting to develop osteoarthritis as well, and grade five, which is when you decide to do a superior capsular reconstruction. This is the Seebauer classification, which is similar, but it has type 1A, type 1B, type 2A, and type 2B. I think the most important thing that's different about these is Seebauer has a type 2B, which is decentered and unstable, where you have that anterior superior escape, which we don't really have that in the Hamada classification. Now, the problem with these is that they aren't all that reliable, and the interrelator reliability is pretty low. So not surprisingly, there have been several studies looking at the accuracy and reliability of these studies. LIPE almost a decade ago found that there was only mild agreement with the Goutelier classification, and there was almost no agreement in the classification of muscle atrophy. A similar study in AJSM that year found only mild agreement with Goutelier, and it didn't matter if you were a general practitioner, a shoulder elbow fellowship trained person, or a sports medicine trained person. They all weren't all that great in terms of inter- or intra-relator reliability. And there was a more recent study that showed a higher agreement with Goutelier, but the problem was there was only 20 patients. So overall, I think that the problems with these classification systems is they're really observer dependent, and they may be decent at best for research, but they're not great for patient care, and they're probably not ideal for necessarily making all of your treatment decisions based on just what your qualitative scoring is. So what our group and several others have started to go towards is more of a quantitative MRI, and there's several different types, and I don't really pretend to know the advantages of the different types. What we have used for the most part is ideal imaging, and ideal imaging is a pretty good measure of fat within muscle where you can get a numeric value for the fat fraction or the percent of fat within the muscle. It was originally described in the early 2000s for fatty disease within liver, and we first looked at it about six years ago and found that there was an increasing fat fraction that correlated really well with the Goutelier classification. Now I have to admit, if you look at the bottom right, the ideal imaging doesn't look all that much different. The arrows basically point to dots that look about the same to me. But the main difference is with automated segmentation, we're able to get a percentage of fat that correlates really well, and that's shown on the left here. If you look at a series of over 100 MRIs, we found that the correlation between Goutelier classification and the amount of fat fraction was pretty good. And then importantly, even in the Goutelier stage four, the actual fat fraction is still only about 25 to 30%. So even though we talk about fat being throughout the muscle and it being mostly fat, it still overall only encompasses about 25 to 30% in the worst case scenario. Okay, so we have better techniques to quantify muscle quality. How can we actually use this to help our patients? Well, we all do apparently have a fair amount of extra time, and I think it's worth going back and reading the series of natural history studies from Ken Yamaguchi and his WashU group that started in the early to mid 2000s and extended into mid to late 2015, 2016, 17. I think Dr. Yamaguchi is one of the great pioneers of understanding rotator cuff disease. Unfortunately, he is a lifelong diehard Dodgers fans, so this is the only slide I'll actually put of him in this talk. And when I think about rotator cuff tears in the natural history, I kind of think about them as three different problems. I think about them as the asymptomatic patients, the symptomatic patients that aren't developing any progressive changes, and then the symptomatic patients that are developing progressive changes and are more on the way to surgery. So we know from many natural history studies that rotator cuff disease overall is often a silent problem. Yamamoto, who's had two really nice studies, performed a series of these studies in a large number of asymptomatic patients. He found that there was a really high prevalence of patients with rotator cuff problems in a normal population and that these tears increased in number and size as the patients aged. Moosmeier, back in 2013, had a really nice study that looked at a smaller cohort over time and found that a third of the asymptomatic patients developed symptoms, which he defined as pain, within three years. Of those, one third that developed pain, a third of those also developed fatty infiltration and muscle atrophy. And enlargement correlated with pain development, and that was consistent in a lot of the WASH-U studies as well, is that when these tears get bigger, that's when patients end up having more symptoms. Now, what about the clinically apparent tears? And if we look back at this patient, we had a 57-year-old male with some symptoms of right shoulder pain and a full thickness tear. In broad strokes, these are the things that I think you really need to know. When we look at our average age at UCSF, the patients that come in with a symptomatic partial thickness tear, they tend to be almost 50 years old. A full thickness tear is almost 60, and the average age of people we operate on is 65 years. Now, when I think about the natural history for these people and what I tell them, I tell them, unfortunately, everything gets worse with time. Most importantly, every single day, patients get older, and we know that healing rates get worse. I tell them that over time, your tear will get bigger, but there are some subtypes of tears that we know now which ones are at higher risk to get injured or to get bigger. And we know that muscle quality worsens and that there are some tears that the muscle quality is going to get worse faster than others. But this is important because that's going to be able to predict our outcomes. So why aren't all tears symptomatic, and why do some patients get better with nonoperative management? Looking back at the Wash U group again, it turns out that most tears probably fall into the rotator cuff crescent. So this was a study done under ultrasound rather than MRI. And they found that a majority of the tears, when they looked at almost 300 tears, most of them fell in the kind of 1.5 to 1.8 centimeter distance, which is right in the middle of the crescent, kind of away from the biceps tendon. And as you get closer to the biceps tendon, as you extend it more farther posteriorly, less and less of the tears were there. So it's probably more of a clinical problem when the tears enlarge and extend either anteriorly or posteriorly and disrupt the rotator cuff cable. And now some patients will have asymptomatic tears. We don't worry about them. And some will be symptomatic with partial tears, and some will be symptomatic with full thickness tears. What patients really seem to want to know when they come into clinic is, are they going to get worse, and what happens if they don't do anything? We know that people will get worse with tear enlargement from a variety of studies, including the 2013 Musmeyer study. And this study was by Jake Keener in 2015, which broke down the risk of enlargement by partial and full thickness tears in two or five years. And they found at two years, only about 10% of patients with partial thickness tears will enlarge. And then your partial thickness tears at five years, only about a third will enlarge. But the full thickness tears are different. At five years, half of them will have enlarged. The bigger the tear, it's more likely to enlarge. And hand dominance is associated with a greater enlargement risk. When we look at enlargement, it does look like there is probably a critical size defect where patients become both biomechanically and biologically symptomatic. Ty Lee's study, where they use probably the most complicated shoulder apparatus to evaluate whether there was a critical size defect in rotator cuff tears, from a biomechanical standpoint, looked at essentially making sequential cuts in the rotator cuff and determined when you lost your abduction capacity. What they found was that when you tore through the entire supraspinatus, the critical size defect, this is where the critical size defect was where abduction capability was decreased. This makes sense when you combine it with the Wash U natural history studies. As you extend out of the crescent and into the cable, you lose your biomechanical advantage. And that's why these patients probably start to become more symptomatic. Now, what about tears that were more anterior? There's a couple of studies that I think are really important to know. This is one study by the Wash U group that was published in 2012. And when they looked at patients that extended into that biceps tendon area, so into the anterior cable, they found that these anterior tears tended to have more pain. They tended to get larger faster, and they tended to have more fatty infiltration. So the summary from these two studies, I think, is that posterior tears probably have more biomechanical consequences. As you go through the entire supra and into the infra, you're probably having more problems raising your arm up, and you're going to have more of a functional limitation. And these anterior tears, as we'll talk about more, not only have some biomechanical consequences, but have biologic consequences in terms of the muscle quality. And I think this study that was published a few years later is really important in how I changed my thought process with rotator cuff tears. What they did was they looked at, independent of tear size, they looked at how the distance from the biceps resulted in muscle degeneration. And they found that if you were more than 10 millimeters from the biceps, you essentially had no degeneration. But if the tear was very closer into the biceps tendon or disrupting the anterior cable, you had a high likelihood of muscle degeneration. And this is very different from what we thought 10 to 15 years ago, where we thought fatty infiltration, muscle degeneration, and atrophy were to be important predictors in large and massive tears only. And this data suggests that certain small tears are going to have more biologic consequences if they're in the right location. And this is just an example that I have from clinic. The patient on the left was very symptomatic. They had really small tears, only about seven to eight millimeters, but had moderate muscle changes in a 55-year-old woman, and really progressed very quickly to wanting surgery and undergoing surgery. On the right is a patient that I followed for a couple years and had kind of just off and on symptoms, and eventually decided to get surgery because it was a convenient point in their life, but had no muscle changes. And even though it was a bigger tear, the actual cable was intact. And I think this is a good example of how that location, even for small tears, may be both important symptomatically and biologically. And what about muscle degeneration in natural history? This is another nice study from Jay Keener and his colleagues from 2015. They looked at risk factors for muscle degeneration and found that the overall muscle degeneration is highly variable. However, most patients, about 80 percent, will show some level of progression of degeneration. And it's much more likely, if that tear has progressed into the anterior cable, that's going to be your number one predictor of whether or not the muscle degenerates. Now, importantly, when I think about when I tell patients to consider having surgery, this study found that the median time from enlargement to progression of muscle degeneration, so you're minimally symptomatic to more symptomatic patients, was about 11 months. So I tell patients, at some point in the next year, if you're becoming more symptomatic, it's probably beneficial to consider surgery. So in summary from this part, I think, from the muscle degeneration part, I think it's important to know that most patients will actually have some level of muscle degeneration. And we've shown in some MRI studies that even with small tears, about 15 to 20 percent of patients will have some fatty infiltration when you look at ideal. And patients over the age of 70, about 90 percent, even with partial thickness tears, will have some level of muscle degeneration. The tears that are at risk are the larger tears, which are greater than 15 millimeters, significant enlargement, which is hard to tell on MRI. Admittedly, it's easier to tell with ultrasound. Disruption of the anterior cable is probably the biggest risk for muscle degeneration. And muscle changes seen within a year are usually seen within a year of that enlargement. So I think so far, what we can say is that the natural history of symptomatic cuff tears is that they will enlarge over time. They don't heal on their own. These muscle changes probably happen early, probably within the first year, which is different than what we thought initially. I was taught when I was a resident in the mid-2000s that it took on average of five years for the muscle changes to happen. Anything that disrupts the anterior cable is probably more important. And that atrophy and fatty infiltration may not be reversible. And we'll get to that in a little bit, but one thing I want you to start thinking about is, well if fatty infiltration is present in most tares, is this entirely a bad thing or would there be some biologic reason why this might be around? So moving into some of the natural history studies in terms of outcomes. This wasn't the first, this wasn't the first paper that necessarily looked at this, but this was the first paper that I actually read when I was a resident. Not the first paper overall, but the first paper that I read that was related to this. And this was the, I thought this paper was really important because it was the first one that really highlighted the importance of muscle quality and surgical outcomes. And what they concluded was that muscle atrophy and fatty infiltration had a significant role in determining functional outcome after rotator cuff repair. They also concluded that successful repair didn't lead to improvement or reversal of muscle degeneration, but that failed repairs result in significantly more progression. So this paper is now 15 years old and it's kind of shocking that in the last 15 years we haven't really found anything all that different. So when we look at other studies, these are additional papers out of Korea that show similar things. They show that the quality of the muscle, particularly fatty infiltration, over atrophy, is a predictor of your healing rates. I also tell patients size of tear, certainly age of patient, but not as much, are independent predictors. Quality of the tendon, which we don't grade yet, is probably important, but since we don't have a good way to grade it, I don't really talk to patients about it. And I do let my workers comp patients know that even though I'm gonna be happy with what their repair looks like, they're gonna be miserable anyway. So now what about if we use quantitative imaging? Are we able to break this down a little bit better? And this study came out about three and a half years ago now, and they used a, they didn't use ideal, but they used a similar quantitative imaging system, and they looked at preoperative fat fractions in the supraspinatus, and they found that they were significantly higher than in our, in the failed repair group than the intact repair group. Admittedly, their overall numbers were pretty high. They had, they had a larger number of large and massive tears, but they concluded that worse muscle quality was, was correlated with a higher retear rate, and just like Gladstone's paper, they found that the muscle gets worse if the repair fails, and it seems almost to accelerate the degeneration. What they had, what they and other groups, including us, haven't been able to figure out is, is there a muscle quality fat fraction cutoff to say, okay, absolutely, a repair is not going to work. Now what about whether or not it actually does improve after repair? Now even though there are some studies, and they're definitely, when you go to Academy or AOSSM, there are going to be people that stand up at the podium and say, well, if I do a double row repair with my techniques, I find that there's a decrease in atrophy and fatty infiltration, and you can see this in these five or seven MRIs. Most of the data suggests that muscle quality does not get better, no matter how do you look, no matter how you look at the data. This study came out in 2014. They looked at over 102 patients, most of which followed up. They had a 30% re-rupture, which is consistent with most of these studies. They found that no patients improved muscle quality. Their fatty infiltration didn't get better, and their atrophy didn't get any better. And again, re-rupture is associated with worse muscle fatty infiltration and progression of atrophy. I thought this was an interesting study that came out last year, two years now, two years ago now in AGSM. They looked at ultrasound-based measurements of atrophy and perfusion after repair. It's a relatively small series, so they had 38 shoulders about three years after their rotator cuff repair, and they had a really high correlation demonstrated with areas with poor perfusion and functional impairment and increased atrophy. And they found that muscle quality was related to relative areas of poor blood flow, which we think is interesting because we're seeing in some of our animal models that hypoxia seems to be a stimulant for stem cell changes within the rotator cuff muscle. Now we've done a similar study with IDEAL, and we found that even with successful repair, so this is a study that Drew Lansdowne did and published in OJSM a few years ago, we looked at 35 patients with IDEAL pre-imaging pre-op and post-op, and it turns out even when we do a successful repair, the muscle quality in terms of fat fraction gets slightly worse. That was statistically significant, but it gets considerably worse if you have a failed repair. So even when we do quantitative imaging, we find that you're going to progress your fatty infiltration even with a successful repair. So, so far we know that symptomatic tears tend to progress. They are going to progress through the rotator cuff cable, which is going to lead to rapid muscle deterioration. This is going to predict outcomes, and muscle quality probably doesn't get better even if it heals. So let's talk a little bit now about fatty infiltration, and hopefully I can keep you guys awake through about five minutes of basic science. Now since this is a fellows-based talk, I want you to think about a couple things. First, how can muscle turn into fat? We know that myocytes are terminally differentiated, and that's not really known as a process that infiltrates. Think about where your belly is sitting on your body right now. It just sits there. It doesn't actually infiltrate. And second is, would there be a biologic advantage to having fat stores within muscle? We think that fat has a variety of different positive things, not just cosmetically, but it may be a significant energy store. Now when I was a resident, what I was told was that muscle is infiltrated by fat, and from a biologic standpoint, that just really didn't make sense to me. But what I was taught was that fatty infiltration happens because the rotator cuff detaches, the penation angle changes, and then fat literally walks in from around the rotator cuff and infiltrates, and then sits there. And it kind of made sense. Like I can draw it out, it looks pretty, and it was, at least if I didn't think about it biologically, a very reasonable explanation. And it made sense because the name was fatty infiltration. More recently, we wanted to figure out if that really doesn't make sense. Are there cells within the muscle or that could be recruited into the muscle that actually turn into fats? And there's a variety of different potential cells that could be responsible for fatty infiltration within the muscle. Myocytes, like we talked about, are terminally differentiated. Satellite cells in some groups, including the old Michigan group that Ashish Bedi worked with, they were able to turn satellite cells into fat, but it's pretty hard to do. Frank Petrigliano has looked at vascular parasites as a potential source, both to stimulate rotator cuff regeneration, as well as a potential cell source for fatty infiltration. We've looked at other muscle stem cells with Andrew Brack, but the ones that we thought were most interesting were these fibro adipocyte precursor cells, mainly because of their name. If they say they're adipocytes, then it may be a good precursor cell for fatty infiltration. Now these are interesting for a variety of different reasons. Fibro adipoprogenitor cells are a resident muscle cell population that not only differentiate into fat and fibrotic tissue, but also can be driven into a pro-myogenic phenotype that resembles round fat. And we think that's pretty interesting because if you have a stem cell source that helps in the development of muscle and then essentially sits there in a quiescent state until your rotator cuff gets injured, it gets injured and nothing really happens. It turns into white fat, but it does continue to have the ability to potentially turn into a cell source that secretes pro-myogenic factors. Now most of these studies were done in mice, and I'm gonna skip over this slide in the interest of time, but we wanted to recently look and see if this actually happens for people as well. And I wanted to bring this up because this was actually something that could, in theory, have been done with a fellow from start to finish. This study took us about five and a half months. So we consented about 20 patients with varying size tears to undergo a small biopsy. We used a little runger at the end of the surgery to grab a few, up to five, maybe not a few, muscle samples, sorted these cells for both FAPs and satellite cells, and then looked at their outcomes. And what we found was pretty interesting. We found that the bigger your tear is and the older you are, the more likely you are to have these FAPs as a significant percentage of the overall number of nucleated cells that are within your rotator cuff. So if you look at the graph on the left, where partial tears, it's about 1%, and then it goes up similar to your FAP fraction with the ideal imaging. So in our patients with large tears, we had anywhere between 12 and 15 percent were these FAP stem cells. And the same thing happened with age, although the distribution was a lot broader. Interestingly, we were able to also see a fair amount of fibrosis, which we don't really talk about, but it's probably important in terms of the compliance and how much you can pull those larger tears over. And what we thought was most interesting is that we can take these cells and we can stimulate them into these pro-myogenic phenotypes, at least in culture, and get them to improve rotator cuff quality. Now when I say we can get them to improve rotator cuff quality, we can certainly do it in a mouse, we can do it with pharmacologic agents, we can do it with cell transplantation, but we haven't yet started doing this for people as of yet. So in summary, I think like we talked about at the start, classification systems are nimble. Quantitative imaging is probably going to become more and more important, especially as it becomes automated. Muscle quality is very important in terms of how patients do, and we should pay as much attention to it as possible. And I'm hoping that over the next decade or so, we are able to leverage the stem cells that are actually sitting within our rotator cuff to be modifiable and improve their outcomes after cuff repair. So going back to this case, and I don't know how the sharing works, but what do you want to do for this patient? He's 57, he's got about five months of shoulder pain. How many people actually want to operate on this person versus do physical therapy? And can you, let me see, and I don't know how to do that part. All right, well I'm gonna skip forward because I don't know how to call on people, and if I call on people, I don't want to call on them. Brian, we can, actually there's a, on the bottom right, in the middle there's a bar and on the right hand portion there's a reaction sign, so if you want to ask a question, and they can do a thumbs up, and we can kind of get an idea of the number of thumbs up there are, if you want to do that. But also I've unmuted a few shoulder surgeons in this list, including Mike Freehill and Will Workman and Steve Cohen, and I thought I unmuted Steve Cohen. I've unmuted the tool as well, even though he's a patellofemoral guy, he's been known to venture into the shoulder, and where's, I'll pull Seth up as well, but if there's another faculty member that wants to, Bryson, I'm gonna unmute you too, and so if you want to have some of some faculty speak up as well. Yeah, so if another faculty would, you know, give their approach to how they would address this patient, I'd love to hear it. I hear, you know, I think Tim's iPhone is Tim McAdams, so Tim, I got you unlocked too. Mark, am I unmuted? You are, Will. Brian, that was fantastic, I haven't met you, but that's really, well, learned a lot, great overview. I'm chiming in because I'm worried this is a trick question, because I see that, and I wish that every single rotator cuff I had was a 57-year-old with a one and a half centimeter tear, because I think they tend to do pretty well when they're fixed. I mean, I, for the reason you said, I, you know, he's on the younger side, and he's got hopefully a lot of years left with that shoulder. You want to give him a chance to heal. I'm assuming that's a, it's a full thickness rotator cuff tear with that. Yeah, yeah, you know, I usually, I think this is an interesting one to talk about, because I think this is what we see most commonly, and the way I was taught was really, this should be somebody that we do physical therapy on, and I would argue that if I, you know, when I took my boards in, I don't know, 2011, 2012, 2010, 2011, if I said I brought them right to surgery, I probably would have had to defend that a lot, a lot more. The reason I bring this up is because of the two studies that came out last year I think are really important, and it's really changed how I talk to patients with rotator cuff tears. So I, I usually tell patients that absolutely we can leave it alone, and for two years and five years, you're probably going to do just as well with non-operative management, or pretty close to as well, but as you get farther out, we know that you're probably going to do better with, with surgery compared to with non-operative management, and if you do a really good study like Nit and Jane did with this study that came out last summer in AJSM, realistically, even short-term, you might do better in the 12 to 18 month category if you have surgery. Ooh, somebody says more, I don't know how to do, fix it, awesome, and a lot of people like my t-shirt, thank you. So what I have started to tell patients now is that nothing gets better than it is right now. You're going to get older, your muscle quality is getting worse, the tear gets bigger, activity levels are going to drop, and today's data really suggests that we should consider fixing it. So I have this whole conversation, I have a really nice single-page paper to print out, I think I'm thoroughly convincing, I'm engaging, and then most patients say that's great, where do I do physical therapy? I think it's still hard to convince patients, necessarily, when they're not super symptomatic, but um, you know, I think the other thing I really try to convince patients is, hey, the smaller tears, they just, they do better, they're easy for us to fix, which is not insignificant, you get in and out of the OR faster, and I'm hoping that with these smaller tears we can eventually progress to the point where we're doing rehab in a faster way, so that patients that don't look at it and go, oh crap, this is a six month recovery process, maybe if we're fixing a lot of one, one and a half centimeter tears, this maybe can be a three to four month recovery process with the right physical therapy, although we're not really there yet. Hey Brian, I would, I would make the argument, actually, to recommend fixing it sooner rather than later, I think Latul is gonna nod for me a little bit, but uh, you know, and the rationale for that is he's 57, right, so like you mentioned, what's gonna happen, this tear is not fixing itself, ultimately it's going to be problematic for him, and, and you know you're gonna fix it at some point in time, why wait, and you know, what are you gonna, like you talked about a little bit, you're gonna wait for the muscle quality to go down a little bit, you know, obviously it's not functioning, he's a tennis player, he's active, you know, he wants to beat Mark Safran on the court, so you know, you're gonna want to get this guy back, and I think, look, I think you can absolutely have that discussion, look, it doesn't have to be fixed, it's small, there's nothing urgent about rushing to do it, but I'd say look, you're likely gonna need to get it fixed, so if you want to wait, that's your choice, but it could get bigger, but why not fix it now? Yeah, I, I agree, I agree with you, I agree with myself, sometimes I try to convince myself otherwise, that maybe I'm being too aggressive, but I really think patient, like I give them, I try to actually just show them these two graphs, and it has not yet really influenced patients too much, but at the same time, right now, nobody really wants surgery. In the interest of time, I was going to go through a second case, because I think this one's a little bit more complicated, so this is a 51 year old gift from Santa Rosa for me, he has new onset left shoulder pain, he notes that 10 years prior to this, he had a cleanup and bicep surgery, though I got to know him after he had a right rotator cuff repair, he was referred to me after his first surgeon got mad at them, when he dropped his tandem bike off the roof two months after surgery, and then had pain, we did a revision open rotator cuff repair, and then everything was going great, until he fell down and tore his PCL, but the shoulder was okay, he wanted to let me know, he landed on the knee, so he comes in now with a new problem of left shoulder pain, he's got full range of motion, but his strength is noticeably decreased, compared to the other side, where he's doing pretty well, he's got positive nears and Hopkins, and he's relatively young, loves biking, loves golfing, and works as a aggressive divorce attorney up in Santa Rosa, so these are his x-rays when he comes in, and he says he's doing pretty well, this was kind of brought up as a, you know, this is also bothering me, let me make sure I get this side right, sorry, this should be as, this should be left and, or this should be left rather than right, but this is his x-ray, so I guess, I don't know if I can, I haven't figured out how to do show of hands, but how many people would want to just start him with physical therapy, or versus get an MRI on this guy? More, yeah, I can't figure out the show of hands, so I'm gonna say most people, congratulations, awesome, now I can figure it out, MRI, MRI, MRI, Brian Lau says sit on it, do stem cell injection, no, Dr. Lau, okay, so we did get an MRI, this is his MRI, and remember, he's not super symptomatic, and what it showed was a, I'm super proud of this, how to get video into, no, Dr. Lau, I did not teach you to do stem cell injections, so it shows he's got a large rotator cuff tear, I would say grade 2 guttale, he doesn't have that much atrophy yet, but based on his, the fact that his head's riding up, he's a hamada stage 2, so what do you think the treatment options for this, and I'll open it up for discussion at this point, this was in early 2020, he did have a pretty rough 2019, he had two cuff repairs, and we treated him non-operatively for his PCL, so he was in a brace and non-weight bearing for six weeks, we can put a patch on it, we can do some PRP, we do the Jason Drago get bone out of his hip and inject it, we do a standard repair, we can do an SCR, which are awesome training cases, any thoughts? Does any fellow know why we would not do a tendon transfer on this person? I guess I can answer that myself, although I'm sure you're all thinking that if you have a subscap rupture as well, which didn't show that well on the imaging, it's contraindicated to do a LAT transfer. There is talk, I think Dr. Warner would do a combination LAT and PEC transfer. And if I remember correctly, he said he did it once and would never do it again. It seems like a lot of surgery to put a patient through. It's a lot to put a surgeon through too. I don't like any cases that go over an hour and a half to two hours. So what do you guys think? Would you try a standard repair for this guy? He's got a pretty big tear. Would you just leave him alone? Or do something more aggressive like a patch or an SCR or a reverse? I guess I'll chime in. Thanks Will. He's kind of at a precarious point with his shoulder. The x-ray still looks pretty good. His shoulder's still well contained, but he's got this big tear. I think without knowing much more, I'd probably counsel him on the options of either a primary or a revision repair versus an SCR at this point with the idea that we're trying to preserve as much of his sort of normal shoulder structure before going on to reverse total shoulder. Sometimes we get in there, that rotator cuff tissue is still pretty good, and we'll handle a repair. Obviously, repairing is not the same thing as healing. But if it's re-repairable, then I'd like to give him a second chance of that in kind of explaining to him the further sequela and the further options if that fails, including reverse total shoulder, which usually convinces him to try another arthroscopic procedure. And then if the cuff tissue's too good when I get in there, or looks too good when I get in there, then have the option of doing an SCR. That's kind of how I would approach it. Yeah. Anybody else? Here, you've got a comment from a person listed as sit-in. Standard repair, and if that fails, you still can always do the SCR down the road or reverse. Yeah. I mean, I think that's totally reasonable for, you know, I think there are a couple interesting things about him. You know, it was his contralateral, it was his other side that had a large tear and then needed to be revised, and we ended up having to open that side. And then I think on this side, you now have a 51-year-old with bilateral, essentially massive cuff tears. And I think this is an interesting person in that we don't really know what to do with these patients. There's something about their tissue quality that's pretty crappy. In hindsight, you know, right now he's about three months out, and I think he's doing pretty well, although I haven't honestly seen him in the last six weeks. But these patients are people that, in hindsight, I think we should probably be a little bit more aggressive with the tendon-to-bone healing. We were able to pull his entire tendon over with a mini-open. I had done a mini-open on the other side, so he was prepared for it, and he did really well on that side. But moving forward, I think this is the kind of thing I probably would augment in some way, shape, or form, either with a patch, like the Regen10 patch or something. I don't really think you need any PRP or stem cells at the time of repair, but being a little bit more aggressive with the debridement of the greater tuberosity, using more anchors, anything to keep, to kind of stimulate him to heal as much as possible, especially when he's 51. But I think in reading the comments that are either coming privately or in general, I totally agree that I think even a partial repair is better than nothing. We know that if we can get anterior and posterior coverage, that might be good enough. I worry for this guy, because we had to do a subscap as well. And what we ended up doing is a arthroscopic subscap. That took a while. There was a fellow that convinced me we should do this as a double row, which I hadn't done before. So that added a little bit of time and swearing. And then we tried to do an open, or we did do an open repair with Supra and Infra, three medial row anchors and three lateral row anchors. We did have to pull pretty hard on the cuff, but so far, when we started his active range of motion, he was doing pretty well. He was able to get up to about 120, 130. Have you gotten any ultrasound imaging on him since? We did not. We don't really have capability to get ultrasound imaging. We have somebody that could, in theory, do it. I'm kind of afraid to do it on this guy, because right now, he's clinically doing well on both sides. But my guess would be that at least one of them will retear within one year. I think that there's something about these patients that we don't understand why their tissue quality is so poor. Even though this is a muscle quality talk, I think that a guy like this, honestly, there's something innately wrong with his tendon-to-bone healing or his tendon attachment at his rotator cuff to be 51 and have bilateral tears. We've never had surgery on this side before, correct? He had had a bicep stenodesis and quote-unquote clean-up procedure, but no cuff surgery, yeah. Can you talk to the fellows a little bit about your rationale for why was ... I could understand if you decide to do the subscap and the supraninfo open, but why do the subscap through the scope and then open? You mentioned that with your revision on the other side. For me, I would either do this arthroscopic or I would do it open, but I wouldn't combine it. What's your rationale? Sure. The rationale at the time for what ended up being both sides is that we were able to mobilize the subscap relatively easily. If I do 100 cuffs, I maybe will open two or three. It's almost always because I can't get enough of a release with the supra to be comfortable. It's the type of tear that I can't do a margin convergence, or as the residents call it, a marginal convergence when I do it. What I found is that if the subscap can't come over and the supra and infra can't get over either, I usually will just do a debridement and let them know that they need an SCR or a reverse. Honestly, at that point, I usually will convince them that they need a reverse because either I'm not great at SCRs or the patients aren't great at rehabbing, but I'm about 50-50 on this. If I can get the subscap over, I will almost always try to fix it arthroscopically, especially if I'm not doing an open biceps tenodesis. If I think for a younger person, if I think making an incision is going to be the difference between success and failure, I will err towards doing a mini open if I think I'm going to be able to mobilize a little bit better, get a few more sutures in. I honestly, part of it is the error I trained. I didn't do an arthroscopic cuff repair until I was a fellow, and it took me six months of fellowship to figure out exactly what I was looking at when we were doing them arthroscopically. I'm still pretty comfortable with a supra and infra and doing the releases and everything open and as much so as I am arthroscopically. That's one of the things I love about having fellows is I can leave them alone, and I come back, and all of a sudden, what I thought was not mobilizable, they have it pulled over to the footprint. I'd just make a comment. You had said something about tendon transfers, and again, having trained with JP, he did a fair number of tendon transfers, and we had done some, and I'm sure he'd done more than one Latin pec because I know there was one when I was there. But those are more salvage procedures. If you can get this thing closed, certainly get it completely closed as you were, it sounded like you had some tension on it. That would always be, I think, the first and best choice, and again, whether or not you augment or not, you can argue as to whether or not the patch might help. I think things like the reverse is a bailout. I think the SCR is whether or not you believe in the SCR and whether or not that'll help you. But I think doing what you did, and I would agree, doing a posterior superior cuff and a subscap, if you can do one of those through the scope, it's a much easier operation. So I agree with what you did. Brian, did you end up throwing a Regen and 10 on there? No. I've only used them a couple times. I've used them for revision cases. Honestly, it's not enough in my thought process yet to have it routinely around, and we don't carry it in the hospital. But I do think the limited data that came out of Dr. Savoie's group, I think it's probably something either that or something like it is probably worth thinking about in some of these more hard to heal type scenarios. Yeah. I'm trying to find, Dr. Freehill wants to ask a question, but I've got him muted. I've got to find where he is amongst all the people here that are asking questions, or that are signed up. So I'm not sure where he went. Bryson, do you have any comments? Or Tim Wang? There's Freehill. I found him. There you go, Dr. Freehill. Where'd you go? I had unmuted you, and you muted back. There you are. All right. Yeah. Hey, Brian. Thanks for the talk. That was fantastic. I just had a few comments regarding all the fatty infiltration, because it's really interesting to think about. So just going back to some of Drew's work that you guys did, showing that even with successful repair, fatty infiltration worsens a lot of times. And then it makes me think, looking at Christian Gerber's great work, that I think that a tip that I would give to fellows, and this is something that I learned with Laurent Lafosse, is just doing these as fast as you can, throwing a couple tapes in and putting down a lateral row knotless anchor might seem like it's a great thing to do. But I think that Gerber's work shows us that I think a lot of times these are not being put down anatomically, and that you really need to take the time to define what the tear characteristics are. And that might mean one anchor. That might mean two medial row, one lateral row. So that's kind of, get your thoughts on that. And the second thing, I don't know how many people saw Martin Snow out of the UK's arthroscopy article this past month about PRP versus normal saline 10 to 14 days after cuff repair. And it was very interesting that even though the PRP did not show any advantage with regards to clinical outcomes or re-tear rate, that the fatty infiltration was better in that group than without. So I just wanted your compliments on that. Sure. So for the first part, I totally agree. Unless it's my general algorithm and my fellows or former residents that are on can tell me if I'm exaggerating this. But in general, I will do a single row repair in two conditions. One, if the tear is so small, I'm basically creating a hole for the anchor in the cuff and it's smaller than our integrated suture passers. Or if it's so big and I'm worried that pulling it far enough over to recreate the footprint is going to re-tear. But most of the time, I try to at least get a second row. We almost always, at least I always tie medially. I have yet to see a quick and dirty lateral row only that I'm happy with. I know that it's fun to do, but the reality is it doesn't take me or the fellows more than about 30 seconds to tie any knot. And if it's taking them longer than that, I'm going to get frustrated and then they get nervous and then I get nervous and then there's a lot of sweating going on. And so I just try to get them to tie the medial row as quickly as possible and then dump something down in the lateral row because it makes it look pretty. As far as the fatty infiltration, I think that's an interesting concept. From a biologic standpoint, we know that FAPs are highly regulated by macrophages. So it may be that there is an interaction between the anti-inflammatory factors of PRP that's now being locally introduced into that area, altering the environment within the muscle that may be changing things in terms of inflammatory pathways and FAPs. It hasn't really been studied all that much overall, but I do think it is interesting. There was a paper that showed a similar thing at ORS just in vitro, that FAPs are able to slow down their adipogenic phenotype differentiation if PRP was added to adipogenic media. From Dr. Brown, the reason to study FAPs is to find ways to turn off their ability to become fat and that could correlate with better outcomes. Yeah, I mean, I think what's interesting about these cells is that depending on the stimulus, they either turn into fibrotic tissue. So if you look at them in the gastroc and soleus, if you do an Achilles tendon rupture, these cells will stimulate collagen production and they'll become fibroblasts. In the rotator cuff and paraspinal muscles, they turn into fat. With the right stimuli, they turn into beige fat, which are little mitochondrial engines that seem to produce things like IGF-1 and folistatin, that at least when we mix those stimulated FAPs with satellite cells, allow muscle to regenerate much quicker. We had a couple of papers published last year that showed FAPs that are just increasing the number of FAPs, stimulate them to improve repair. But if you kind of drive them towards this beige fat phenotype, that it can take at least in an animal model and put them pretty close back to normal. All right, are there any other questions? Here's another one. Just another thought about fat degeneration on rotator cuff tear. It is known that nerve injuries can occur in muscle fat degeneration, which makes me think about the possibility of the involvement of suprascapular nerve. So can you comment? Obviously, J.P. Warner had looked at releasing the suprascapular nerve and looked at the tension on the nerve, certainly with retracted tears and the effect of release. So do you want to comment a bit on that? Yeah, I mean, I think it's an important factor. I definitely think there's a denervation or an alteration in innervation component to the development of fatty infiltration. We found it's hard to study in lab. We know that if we just do a tendon transection in our model, we get a little bit of fatty infiltration. But if we cut the nerve, we get a marked amount of fatty infiltration. And we had a rather talented microsurgeon for a year or two, and he was able to repair the nerve six weeks later, and we would see the fatty infiltration disappear. That being said, I can't say, I think probably what happens in some of these tears is that the denervation is probably an additive effect. I think the mechanical unloading stimulates some differentiation into fat, but then the denervation is essentially a second hit to these cells. I do not look at the critical shoulder angle. So for Dr. Wong, I don't really look at the critical shoulder angle, and I don't really use it in my clinical decision making. I honestly try to give patients the best advice I can, and I tend to be pretty aggressive in telling patients. I try to err towards telling patients, let's try a repair. I can always do a reverse down the line. I think that's a wise approach. Well, that's great. Brian, thank you so much. That was a fantastic talk, very high level. Really appreciate all the work that you've done in this area, and you're sharing it with everybody. So that was right on time, which I think is also awesome, and thank you all, the faculty, for contributing. Next week, just so you know, the four talks, Lyle Kane from the Andrews Institute will be talking about how to define return-to-play criteria after ACL reconstruction, Ned Amendola from Duke about cynosmotic and Les Frank's injuries, Steve Cohen on Wednesday about hamstring avulsions. He's done a lot of work in that area, and then the last talk, actually, of the week is not going to be me. It's going to be Mark Miller. We'll be talking about revision ACL. So I thank you all for participating. Again, this will be on the AJSM website next week. So thank you all, be safe, and have a great long weekend. Thanks, Brian. You're muted again. All right. All right. Thanks, Mark. Have a good day. Take care.

muscle atrophy

rotator cuffs

muscle quality

predicting outcomes

rotator cuff tears

classification systems

quantitative imaging methods

muscle degeneration

fatty infiltration

early intervention