There we go. Those are my disclosures. And I think that, you know, Nick talked about this, but this is an important concept to understand is that even when we have what we call a healed rotator cuff, it's not really healed. That enthesis, the normal enthesis is never created. So that normal enthesis is a highly organized calcified cartilage, uncalcified fibrocartilage, tendon bone, tissue that normally is there is really disorganized collagen and scar. So it's not. So we're going to just kind of go through all the little biologics that we have that you may hear about, just to go over things to make sure everybody kind of gets a good idea. Definitions, I think it's important. Leukocyte-poor platelet-rich plasma, really good for joints and all things related to healing. Leukocyte and platelet-rich plasma, good for chronic wound care, chronic tendinopathy, state of non-healing. This is where we get into it. You can see the overlap between the platelets and the white blood cells. They're close. So when you're doing a density gradient, how you separate these out either by centrifuge or density, you can see if you want more platelets, you're going to get more white cells. These are all the growth factors that are contained in the platelets. All of these protein signals that are ubiquitous to all aspects of cellular growth. So these all alone do a great job of healing things. However, the dose and the time when they're executed is critical. If they're not at the right time or they're too much or too little, then they don't work. Also there's been a lot of talk on the variability of PRP when it comes to rotator cuff, and that's because patients are variable. So when you're talking or going with biologics, you want to keep in mind that patients are variable and you're going to see that. So these are a group of people at day zero, day 14, and day 35 going with a plasma-based system and a buffy coat-based system, and you can see that none of them were the same ever. Can PRP act as an anti-inflammatory agent? Yep. We found this, and this is very helpful, I think. We talked about it the other day in our biologics section. Does PRP have the potential to protect cells against damaging effective steroids? We were in the biologics section yesterday. There was some work done on cartilage, and you can see here that there's a protective effect of PRP when you mix it with the steroid. There's equal amounts of literature pro-rotator cuff and anti-rotator cuff. So because of that variability, you're going to have literature that goes on both sides of this. That shouldn't dissuade you, I don't think. We know there's variability in all of this. There's also variations on how to collect PRP, as well as variation in patients. So there's a lot of variation in trying to figure out how to compare all of these is a little difficult right now because we don't really know the end goal. Bone marrow aspirate, there's been 203 PubMed papers since 1996. There's three autologous sources of bone, and when we're talking about mesenchymal progenitor cells, we're talking about lower on the line so they can differentiate into chondrocytes, fat and cartilage. And that's how you tell if they're progenitor cells. There's different ways to obtain bone marrow. There's the crimson duvet. There's vented anchors. There's a lot of different ways to prepare concentrated bone marrow. Scott Rodio talked about a study yesterday where the iliac crest had more progenitor cells than the proximal humerus. But I would just argue that we don't know how many cells we need or why. These are recent articles, Nick Verma's article here in AJSM 2023 randomized trial. So adipose, Pietro Randelli from Italy has done a lot of work, some good randomized prospective studies looking at how you can take fat, and it's very promising. Kim et al. in AJSM also found excellent. And then intraoperative injection of adipose tissue was found to be safe and effective in humans. That's another article by Randelli in 2022. Adipose derived mesenchymal stem cells improve structural but not clinical outcomes. That's really kind of similar to what we've seen in most of all the papers right now. Intraoperative injection, amniotic membrane. This I just put in here for completeness. I don't know much about it. I know that the idea of the amniotic membrane is it has healing without scar. Which may work, but since we're looking for scar formation to heal our rotator cuffs, I'm not sure how that's going to be. Bursa, I think it's cheap, easy to use, very close. It's been around, I mean, everybody knows it's been around for a long time, but they've talked about it for a long time. Uthoff really wrote an article saying you shouldn't take it. And then Neer started talking about the subacromial decompression. The reason why we got into this bursa is because there's a lot of basic science literature that shows that tendon healing really comes from the paratenon, not necessarily the bone or the tendon itself. So those cells migrate in from the paratenon. We figured that the paratenon of the rotator cuff was the bursa. That's how we got going on this. Biologic activity, it really has more colony-forming units at a faster time than concentrated bone marrow. You can see here when we're looking at proliferative ability, bursa is significantly greater than concentrated bone marrow at day 10. And then you can see the pellets with the bursa over the tendon, bursa over the muscle versus concentrated bone marrow. It's just slower. We did an article where we looked at in a mouse model how the healing and what the mechanism would be, both when we grew up the cells and put them in, and then when we did a point of care and found that we had significantly successful rotator cuff repairs. However, in the mouse model, for those of you that work in the animal world, they heal everything. Bursa has two different areas, bursa over the tendon and bursa over the muscle. You definitely need to break it down to get it out of and to have it. If you just leave it, it won't really release its cells. You have to bring them down. There's more cells in the bursa over the tendon than in the muscle. Really the cellular concentration of the bursa is really dominated by progenitor cells and fibroblasts. When patients are indicated, we're really trying to prevent the failure, the primary failure of this. So the age, the tear does not make a significant impact on the cellular content of the bursa. Really we do a 3-to-1 ratio of PRP, PPP to autologous thrombin, and then we mix whatever bursa we get. We usually take about three centimeters of bursa to mix that. I think all biomechanical studies or talks on rotator cuff should talk about really kind of the basic single row versus double row. We beat that horse to death, but I think it's always good to try to go over it again just to make sure. What we found was that in a double row, even though the contact pressure decreases, if you start with a greater contact pressure in a double row, then you end with a greater contact pressure as you can see in this study. All repairs lose pressure but the double row starts higher and maintains a larger force over time. No difference in clinical outcomes but lower re-tear rates. If tear too big or under tension, then margin convergence. This has kind of gone away and I look forward to talking to everybody about this. Because it's not talked about much anymore. But it's still a treatment that you can do to try to just keep the patient's own tissue in there without working with any of those patches. This was a biomechanical study we did where we looked at taking off the entire supraspinatus and then margin converging it to make sure that it didn't decrease the tension or the strain. And also decreased strain at both zero degrees and 60 degrees of abduction. Massive tears in the SCR. I will say we had a conference in Boston at the Isocos and I will say that the superior capsule reconstruction that Professor Mahada does is completely different than the superior capsule reconstruction that we talk about. I think that has a lot to do with why it's not working out as well in our hands. This was an SCR compared to lower trap transfer by Warner. SCR compared to lower trap transfer. I'm at MGH with both Basim Elhassan and J.P. Warner. So we do a lot of lower trap transfers. The real issue is when you're talking about biomechanics, it's about the force of the deltoid. So when you decrease the force required to move the deltoid, then it moves more. So all of these little procedures that we do, the balloon, the SCR, margin convergence, all of them really created an ability to let less force on the deltoid to give more motion. This was just showing that a loose graft really doesn't help you as much as a tight graft. You need to be able to hold it at 60 degrees. Thick patch is definitely better than a thin patch, so double them over. And then what Mahada uses is his autograft. This was just us using a 3 and 6 millimeter patch and you can see the difference. Lower trap transfer, this is an article that we did for Basim Elhassan. This is just a real, this is a very straightforward operation for him right now. Use Achilles allograft, puts it through, places swivel locks anteriorly, splits it, pulvertafts through the lower trap and that's it. So biologics have a lot of promise, but all have limitations and issues. There's PRP, concentrated bone marrow, adipose, amniotic and bursa. Biomechanics, these are time zero analysis and do not incorporate any type of healing. Key areas to decrease the force needed to the deltoid to raise the arm, double row, single row, margin convergence, SCR and lower trap transfer. Thank you.

biologics

rotator cuff injuries

enthesis

platelet-rich plasma

joint healing