Thanks for having me, and here's the biology talk, which is going to do nothing but make this more controversial. But that's where we're at here with rotator cuff surgery. Because I think the first thing we must ask ourselves is, why talk biology? And maybe it's because we're at this era now where we've done everything to improve our suture strength and our implants, as well as our configurations, but we're still not quite there yet with our results. So the question is, can we add to that in any way? And maybe the biology might be an answer. Biology can be in many different forms, which we'll talk about today, one of which is the PRP growth factor group. The other is scaffolds, and I'll only touch on that because the previous authors have done such a great job discussing that. And finally, the cellular therapy previously known as stem cell therapy. Well what about PRP? What are we going to do about this? And I think the best way to understand this is with a Vangs Ness great review article. All things taken into consideration and using only one level one evidence, greater than 1,000 patients, we can reach the following conclusions, which can either be really good or really bad, depending on how you think of it. Number one, no difference in functional outcome. I want to ask you all, is it worth the $600 to $900 for the PRP if we're not going to have an improvement in our functional outcome? Well, what if we do have decreased long-term retire rates in the PRP group versus control? Is that worth it? Maybe. Maybe it's worth the $600. And here's where the argument lies. If you are in the camp of the pro-PRP, know that two things are associated with improvements. Number one, leukocyte-rich PRP, the stronger kind of PRP to stimulate a reaction. And the second thing, and this is going to be a recurrent theme in this talk, which is different than the previous ones, the biology is placed in the bone interface, in between the bone and the rotator cuff interface. So it's this fundamental argument then, if PRP is not quite strong enough, how are we going to really get improved rates? And Scott talked about it. We need cells. And if there's anything that's lacking at this interface, it's the cells. So how are we going to do this biologically? Well, by far, the number one answer in modern day rotator cuff surgery is to improve the bed environment, to do the crimson veil or the bed abrasion technique, even a microfracture to stimulate the local cells there in the proximal humerus to add to the cellular environment. What's the data? Well, lots of studies here, not a lot of level one evidence, but a lot of studies that suggest the same thing as the PRP. No difference in functional outcome, but a marked difference in retail rate. So then you can see how this pendulum is swung to maybe free biology versus the PRP biology where you pay, of course, for the PRP kit. And that is the reason probably why this is more popular in modern day practice, but same outcomes as PRP. But I want to bring your attention to patients like this. Do you see this rotator cuff here and do you see this zone of high T2 signal here immediately below the bed? This has been correlated on MRIs with decreased cell composition. So therefore, if you're going to do bed abrasion in a patient like this, be careful because there's much less cells there. And you may consider a technique such as micro drilling with the understanding that most of the cells reside seven millimeters below the bone interface. So it's more than the microfracture pick and certainly more than the bed abrasion and especially in these certain patients. But I think Hernegow gave us some really good evidence even way before this to say that when he measured cells in the proximal humerus with a tear, they were about one half in comparison to the patients that didn't have a tear. Well, here's the cell evidence, right? This is at least where we were at as of last year. This is the Hernegow article and I know in rotator cuff rounds, this is something that's been talked about again and again, but let's embrace what it shows. Number one, 10-year follow-up, reasonable amounts of patients, 45 each, and despite some potential bias, twice the healing and four times the chance of a clinical outcome. Well, let's look into this a little bit more, but I think what we can say is, okay, Hernegow, that's reasonable, but before we put that in our practice, we need another study at least to confirm your findings. So again, adding to this controversy, here is one of his videos that shows that he is placing the cells where, not on top of the rotator cuff, but in the interval in between the tendon and the bone. The good news is maybe that that's where our biology belongs and so therefore that may add to the result. The bad news is what you saw, the bone marrow concentrate went everywhere. So from the biology perspective, can we even take one step right now to improve those biologic results and the answer is maybe if we just activate the BMAC and that's by placing thrombin or calcium with your mixture, which creates a gel, which can hold it in that interface for a longer period of time. Well, good news, thanks to Brian Cole and Nucleal Verma, because they have now a randomized version of Hernegow's finding. They did the same thing in a randomized way, rotator cuff repair and rotator cuff repair with BMAC. Where did they place it? Between the bone and the rotator cuff. What's their results? This is going to sound familiar. No change in functional outcome. But what they did show is from a sagiasaurus, much less of a re-tear rate and improvement in the thickness of the tendon. So there's something about this process here in a randomized way, which shows that it may be beneficial. And I don't know if we're there yet. I just talked to Brian Cole. I said, well, how'd you place your BMAC in there? He said, well, I used the same technique and it squirted everywhere. And still, that's still beneficial probably, right? But we might be able to take this to the next generation by even just making a gel concentration over there. So stay tuned as this story unfolds. Again, I didn't want to take much time with regards to scaffold, well discussed previously, but I want to discuss this briefly from the perspective of biology. Number one, the augmentation versus the interposition, as Allison talked about. But from a biologic perspective, there may be one other version. So Allison's version is lengthening a tendon that otherwise wouldn't go back to a footprint. But what about the other kind of interposition that we may do, which we're terming interposition two, which is placing a graft below the area of the interface where biology is necessary. And hence, here is the controversy in comparison to what Scott talked about. I briefly want to say this for reasons. Number one, human allograft, reasonable evidence of a benefit. So we'll leave it at that. Number two, porcine xenograft, in even its bioinductive design, reasonable evidence. I want to acknowledge the fact that even when you put review papers to the xenografts, two things, significant improved outcomes and low complication rates in the literature. But I also want to acknowledge that from a biologic perspective, complications occur with xenograft, and if you look in the literature, they're there. And I think Buddy Savoie maybe summed this up the best when he said, you know, if you use xenografts a lot in your practice, you're going to see it. It's not common, but you're going to see it. My question is fundamentally, do we have the biology of xenografts figured out yet? And maybe the answer is completely no. But I want to spend just a little time talking about biologics and scaffolding in this great paper by Gus Mazzocca and Bob Arciero. They did what is the logical next step. They took human allograft, which has reasonable results, and they added biology to it. They added PRP and they added BMAC. And so then we can expect greater results, right? Wrong. And the question is, why? We're improving biology. Why can we not get the results? Now please don't see this as a criticism of this great study, because it's not a criticism. But we have to think through this as a group. What happened to the biology and why did it not help? Well, it could be their tough patient population, right? Because they all failed primary repair. So this is more of a salvage. Number two, they took the BMAC from the proximal humerus. Well, we already know that that's a site of much less cell origin. And if you compare the numbers, that's well below the iliac crest. It could be number two. But number three, their biology is above. And the question remains and is unanswered, is, is that where we need our biology? So in summary, maybe going forward, I think Scott is right. Scott Rodeo is right when he said, we can't have a graft in between because it's a barrier. But if we choose a graft that grows away, even within hours to a day, and we implant our biology in this graft, maybe we can improve things. And maybe this is the next vision of how we can have a biologic graft. And a matter of fact, early studies, and these are just in the animal models, which show this different interpositional two type of design, have promising results. But of course, stay tuned for results in humans. So in summary, the scaffold controversy is not going anywhere. It could be useful, but not in all of our patients. But I think the thing that is here to stay is giving attention to our rotator cuff repairs and thinking biology from the beginning. Thank you very much.

rotator cuff surgery

PRP growth factors

scaffolds

cellular therapy

functional outcomes