Thank you. Thanks, Cameron. Okay, last, I think this is the last one. The use of orthobiologics as an adjunct to rotator cuff repair. So why is there a need? You know, if you just look at soft tissue injury in general from an epidemiologic point of view, there's somewhere in the neighborhood of four and a half million sports injuries a year that come to our offices. I think the thing that's more interesting is the fact that when you and I repair a rotator cuff, up to 40 to 60% of them will re-tear at anatomic follow-up at one year. And if you, I don't know if any of you have read Being Mortal by Atul Gawande. He talks about this concept we're kind of rotting from the inside out. That's kind of what's happened with the rotator cuff. Most rotator cuff tears that we see in the office setting are really due to degeneration, age-related changes, and have nothing to do whatsoever with trauma. So we're perplexed when we do a great job anatomically and put it back and then we see a re-tear at one year and really all we've done is temporize things and it re-tears the same way it tore in the first place. So I think this is an area where biologics might have a significant role if we can kind of figure it out. The issue with rotator cuff tear is that we're dealing with chronicity. Sometimes it's multiple tendons with no stress shielding. Advanced age has some direct relationship with outcome. Smoking has been definitively shown to be a negative prognostic factor. And then other comorbidities such as diabetes and acute inflammation with inflammatory arthropathies and so forth. So the bottom line is we're dealing with a situation that has compromised biology. So surgery often is not enough in this group. And this is an area that I think is really primed to consider the use of biologics. What we'd love to get is tendon regeneration. And this is really like, it's a calcified layer, it's fibrocartilage. It is a really well-organized insertional structure. And the problem is that when we repair it, most times what happens is we just get reactive scar. If you look at virtually any animal study, it's essentially scar and continuity. And we don't recreate the emphasis. And there's truly a lack of mineralized fibrocartilage. So why does it happen? One of the main reasons, and I think Arnie alluded to it before, is that we deal with inflammation and we love healing by scar, right? This is a situation that I think it's a negative attribute due to the inflammation we heal by fibrosis rather than true tissue regeneration. And unless you get sort of some reversal, if you will, of the disease state, I worry that we're never gonna accomplish anything more than a transient repair for some of these more chronic and challenging rotator cuff tears. The problem is right now, as far as what's available, it's fairly limited. It's really PRP and bone marrow concentrate that we're looking at or thinking about. So I'll just give you a case example of a guy. 51? Which shoulders? Right shoulder. Are you right-handed? Do you have volume up there or do I have it here? I'm maxed out here, unless there's one up here. This is a 51-year-old. He had an acute right shoulder dislocation while body surfing, underwent closed reduction. And really his biggest complaint was that of pain and weakness. All right, so you get the idea. And by physical exam, he has some ecchymosis there because he also ruptured his biceps. He has, you know, I would say a lag sign. You don't know because he's got so much pain, but he really truly has lag signs and abduction, external rotation. So you know he's got something significant. Radiographically, he's normal. So certainly there's no suggestion that this is a chronic problem. By MRI, the quality of the muscle is actually quite good. And as you go laterally, I guess you would say this is probably acute. You look at his age. In the absence of pre-existing problems, I would bank that this is relatively acute given the quality of the muscle there. So, you know, what was done, we could discuss all day long how to repair this, but my preferred technique would be some type of double row technique, transocyst equivalent. But the real question of the day is, do we add anything else to it? Because this is an acute tear. Tissue quality, pretty good. Would you use it in acute setting? We can talk about it in the panel. Or would you only offer in a chronic setting? And I'm not sure the literature really tells us what's best. We have the most literature to date on PRP, a little bit of literature on bone marrow concentrate, and nothing real, to my knowledge, with adipose or amniotic tissue in the surgical setting. Basically, we know there's two essential categories for PRP. And what we often focus on is the leukocyte population, whether it's rich or poor. So that was something that we were interested in in one of the studies that we looked at. Most of the literature actually looked at normal tissue and said, let's look in culture. And culture for tenosites is very difficult. So what we basically did was a retrieval study where we looked at diseased rotator cuff tendon and compared leukocyte poor to leukocyte rich. And there was a belief based on our outcomes that we saw greater collagen synthesis and decreased cytokines with matrix degradation inflammation with our leukocyte poor product versus leukocyte rich. And again, that was a diseased tendon, not normal tendon. So we thought that was really important during the analysis. The other potential advantage for PRP in this application is that you're denuding the bone, you're performing on a chromioplasty, is the ability for PRP to signal for MSCs into the area. So there is pretty decent data there that it may function in that role only and less about the growth factors acting locally. So there's that added benefit. There's some other really interesting data when you look at just this concept that Steve Snyder's popularized as crimson duvet where you just denude the surface and maybe even perform a marrow stimulation equivalent there. And it's interesting, there's pretty decent data looking in a comparative trial at marrow stimulation to control with anatomic integrity at one year. And that it's also benefited to tendon repairs when you do marrow stimulation. So this would be the sort of the poor man's PRP suggesting that it might have some impact. We and others have looked at this both directly through our own studies and as well as through systematic reviews. I think the take home now is that fiber matrix may not be beneficial, but injecting locally when you do a double row repair and small to medium sized tear may make a difference. So when you try to summarize all the data, there's 32 studies, 21 randomized trials, three of them are conservative, 18 of them are surgical. And I think the take home is, I'm not really ready to say it's a dominant treatment strategy, but there clearly is a suggestion as of 2018 that if you apply it at the tendon bone interface with a double row repair, comparing with and without, that small to medium sized tears seem to have a increase in anatomic integrity at one year follow up. So it's interesting, we're still trying to figure it out definitively. There's a number of bone marrow concentrated systems. This is a study that made me start thinking about, look, maybe we're not thinking about the entire picture. It's not just what we're injecting, but maybe we'll need a scaffold, maybe we'll need cells, maybe we'll need growth factors. And this is a study that did look at that and said, look, in conclusion, it's not just the soluble factors, but we may need cells, we may need scaffold. And in order to get it done, especially when it comes to a cuff, it's probably gonna take something more than just an injection. This study is particularly compelling because they had 45 patients with and without, and I alluded to this before, using bone marrow concentrate and they had a profound difference at 10 years. We're in the process, and I'll just share some early data with you. This is a prospective randomized controlled trial with multiple investigators, all aligned with the same surgical technique. A single tendon tear using trans-acid equivalent repair, half get it, half don't. Everyone gets a needle stick, so they don't know if they're getting it or not. Currently we have 27 patients, this is kind of hot off the press, 27 patients who have had bone marrow concentrate, 34 that have been treated with a sham. So we're doing an MRI at 12 months, and I'll just give you the anatomic data because we haven't really looked at the clinical data now, but 35 patients at 12 months with MRI. And I think if you just look at the last point, the Sugaia score, that's essentially the lower the score, the better. So partial thickness, signal change, things like that in MRI gets a one, and as you go all the way up, you go up to a four or a five. So we have, it's very early, so consider this pilot stuff, but we're powered for significance, but right now we're only at 35 patients. But there's a strong suggestion, and we even reached statistical significance at this point, that bone marrow concentrate is doing better in the Sugaia classification than the control group. So I think it's important to redo Hernegow's study because it was a case control, and I think hopefully by next year we'll have something to definitive report. So here he is, early post-op, nothing like long-term follow-up at two months, and he was doing great. And in this case I actually gave him bone marrow concentrate and he was part of our study. One other thought I'll just leave you with. I think the real problem is not necessarily the tendon itself, but it's how the bone grows into the tendon. So one way to really think responsibly about this is maybe we should consider ways to augment the bone-tendon interface. So I've become particularly interested in the use of maybe using some type of demyelized bone matrix or other at the tendon interface to sort of help recreate that fibrocartilage transition zone of tendon into bone. It's something that's compelling. Not every study has shown a difference, but some in the animal world have shown, in the preclinical world have shown significant differences in biomechanics and histology. So in conclusion, rotator cuff tears are associated with poor tendon biology, and truth be told, they're largely degenerative. They heal often with scar and continuity. They have very poor material properties, even if we can improve the structural properties. And I believe the growth factors are not really gonna be enough. I think we're gonna need something else that's signaling for and sort of licensed to recapitulate the emphasis. And I think we're gonna probably need cells, we're probably gonna need growth factors, and we're probably gonna need some type of scaffold that has biomechanical integrity. And that's ultimately what's gonna give us what we need for a durable repair. So I wanna thank you for your attention. It's been a great night. I know I've learned a lot. So thank you for your attention. Thank you. So it's 8.06, and I think what we'll do is we're not really that far behind, which is nice. Why don't we have the panel come up? We have plenty of chairs, and let's, if you guys have questions, go ahead and use your mics, and let's start there. So if you guys would come up. Why don't you go ahead. Can you put on your MBA hat? You're the head of your surgery center, and you wanna use Regenitin. You see Dr. Savoy's beautiful picture. How do you know how to use that, and how can you justify it? We're taking money out of the system for basics. So from an MBA standpoint, what proof do we need to say that Regenitin is great? It's funny. I had a conversation with a woman who just went on to practice. I think she's in California, and she's saying, well, look, isn't it the right thing to do even if you can't get paid for it? Yeah, it probably is the right thing to do for some of the things that we do, but we're fiscally challenged. So you asked me for my MBA hat, and I would say that my understanding of the literature, while I have seen these pasta partial tears show, you know, I've talked to Steve Arnosky for hours about this, and he would say that it might be conductive. So what he's talking about is a processed collagen membrane that has virtually no mechanical integrity, that really has excellent instrumentation to put it in, that might be conductive, quasi-inductive, but the initial studies showed that when you place it on top of a partial thickness, classic pasta lesion, that you see changes in MRI over time. So it's magic, right? So it was compelling because you take a problem typically occurring in a very challenging individual, like an overhead athlete, who you really don't want to do a formal rotator cuff repair, because that's sort of the kiss of death, especially in a thrower, so we would typically debride them. So it offers an opportunity. The challenge for them from their business model, in my opinion, is, and that's not the subject of this course, they're not even really, there's no, they're not represented here as far as I know, but is that that's a small population of patients. And so that model of treating a pasta tear with something augmented to get it to fill in without a formal rotator cuff repair has been extrapolated to the majority of it's being used in full thickness tears and even revision situations. And it's compelling because the instrumentation is super easy and you can do a patch augmentation. It's dissatisfying economically because we don't really have a true reimbursement pathway, much like SCR, which is also challenging, that we're fighting to get reimbursement for use of combining different codes. So for you, it's challenging because you won't, you may not get paid any more than rotator cuff repair or it'll allow you to bill for rotator cuff repair when you otherwise wouldn't do it. So I guess that's thumbs up for that. So from the surgery center's point of view, it's, I think, if you ask me, is it evidence-based enough to say it's justifiable? My answer, my personal answer is no. So I started using it because I was interested. I wanted to see how it was from the instrumentation point of view, as gratifying technically in the operating room. But I think from a fiscal responsibility point of view, you need sufficient data to make that decision. So in my surgery center, where I, with my partners, I would just discourage it because it financially is really challenging. So that's my answer. You asked me the business answer. It's really, some of the stuff is pretty compelling by MRI and so forth, but until we really know the difference clinically, I'm not there yet personally. So that's my answer. Did you consider using that case you showed because the tendon didn't look that great? So the place I would use it is someone who has a legitimate partial thickness tear where there's disease beyond that, okay? So I've got some really interesting cases, much like Buddy shows, where there's disease in the tendon beyond that maybe focal thickness area, where it's almost like cartilage injury, where you know the zone of injury is much greater. That, to me, makes a lot of sense based upon what I've seen. That's a good patient. And I would have no problem using it in a high-level athlete where the alternatives are really unpredictable at best. So why don't we move on? Go ahead. Thank you, great question. So a question for Dr. Kaplan. We've heard about the, we've heard about BMAC and colony-forming units, and I just wanted to close the loop on that. Is there a direct correlation with the number of colony-forming units? Should we be measuring that with an aliquot in the clinical result? And are all the colonies the same, or are they different from progenitor cells? Well, so it depends what you're gonna use BMAC for. If you're gonna put it into an osteoarthritic knee and you think some MSCs are gonna make cartilage, you're way off. So what's been shown in animal models, and what's crystal clear, is you can put a gazillion MSCs in wherever you want, they're not gonna differentiate. They will, there will be some cells in BMAC that are osteogenic that actually are very useful for bone repair, particularly complex fracture repair. But that's it. You can get osteoblast, you can get some bone, but you're not gonna get cartilage, tendon, fat, any of those, quote, tissues that you think you're gonna get with that. So the colonies don't have anything to do with what BMAC is doing. BMAC, first of all, hemopoietic progenitors, which are the majority of cells in BMAC, are professional secretory cells. So they're making all kinds of goodies and pouring them into whatever site you put the BMAC. So those are the cells that are making cytokines and growth factors and agents, and who knows who's the active member of that symphony. So it's not the MSCs, because again, if you take 10 mL aspirate from a 50 year old, that's how many MSCs you got in there. So you can show as many colony forming units as you want. It's not gonna give you a potency of therapy for BMAC. So those of us who work with purified culture expanded MSCs, likewise, don't have accurate potency assays for the use of those cells. So we're still experimenting with dosing. But I can tell you, the biggest MSC company in the universe is Mesoblast. You can go to their website. With a very long needle, they showed that six million marrow culture expanded allogeneic MSCs in low back pain and patients that respond can give you three year outcomes of fabulous pain relief. 50 to 60% of the patients, by three months, you can already identify as non-responders. So we know the MSCs are working. And we know that six million cells is twice as good as 12 million cells, I might add. And that's Mesoblast data. The issue is, in our business, that we know there's an inordinate number of non-responders. So Mesoblast uses the same MSC for acute myocardial infarcts, for diabetes, for low back pain, and for graft versus host disease. So the cells are not tuned to the disease. That's number one. And they're not tuned to the patient. So you get bone marrow MSCs from you, put them in culture, and then you give them to me. I don't like your MSCs. My genotype isn't compatible with responding to your MSCs. So as an industry, we're having to learn, A, how to tune cells for particular diseases, and B, personalized medicine. And so that's even further. We're dealing with purified MSCs in these examples. And we already know that in the perfect case, not BMAC, in the perfect case, 50% of the people are not responding. And I would just point out to Brian, for AAOS and for this society, that I just wrote a paper to suggest that we use the non-responders instead of placebo controls. Because they're the floor of the clinical response. And we better get more than that floor to get a really good clinical response. And as we all know, in orthopedics, saline is one of the best clinical drugs that we have for a variety of issues. So again, cell-based therapy, and how to dose and what preparations are best et cetera, very difficult now to give you precise answers. Colony forming units is not a predictor of potency of any of those marrow preparations, zero. So it's looking at some, what's it measuring? Well, it's measuring, MSCs form colonies, they're adherence cells. So I can tell you in all the studies that I've published, and I've published the study that shows the decrease of MSC of age, those are estimates. Because there's MSCs that we know are in the preparation that don't plate out. Because we can do subsequent tricks to get them to plate out. So all of those are estimates. And colony forming units are a way of giving you a quasi-quantitative estimate of the number of MSCs in a marrow prep, or in a preparation. But it's not a definitive. So just, I liked, it was a great question. We're trying to drive it home. So is the narrative that if there are MSCs and you're getting some efficacy clinically, it's not coming from the MSCs when it's bone marrow concentrate, it's some other hematopoietic element. Is that where you are? Because the number of true cells is so infinitesimally small and they're not behaving in any way that, you know, from your first paradigm. You're putting 30 million marrows, 30 to 80 million marrow cells into a injury site, and there are five MSCs. Where's the message there? Yeah, I just didn't have that same take home. When you look at CFUs, when you look at gating, when you're trying to measure what cells are there with receptor positive, negative, and so forth, I had a different take home. I'm not questioning the mechanism, who's working when. I'm just, my understanding, unless all these papers are saying something different, that at least the number of cells were identified as MSCs was much higher than that. There are 600 clinicians and clinics that are advertising on the web for stem cell procedures. There are two orthopedic surgeons in Cleveland who I personally would like to strangle who do full page ads for stem cell and regenerative medicine treatments. Their two products are BMAC and PRP. They're not, and all of their text is taken right from the MSC literature. So it's an MSC text with two products which are not MSCs. Jason, do you want to say something? Well, the colony forming units are a research tool to prove that MSCs are present, and that's valuable because we are taking a body's tissue and we are rearranging it. We're mulching it, we're doing something to it, and then at the end of the day, what do you have left? And if we didn't have tools like the cell sorting and the colony forming units, we could not prove that at least at the end of our procedure or preparatory procedure that there was something there. Right, so that they're there and they're able to do the job of an MSC, right, because they're sticking to the plate, they're cloning themselves, et cetera. But I agree totally with Dr. Kaplan, that has nothing to do with their clinical efficacy. And I think that's what you're saying, right, that they're there, you're proving it. Some way we have to prove them via research, right? If we're coming out with a new product or a new technique, somebody's got to know, but that has nothing to do with how well they work or the job that they do in the body. Yeah, I agree with you, but I think in osteoarthritis, I think it'd be more productive to do an ELISA for IRAP. Because you know that that's an important molecule. The number of MSCs doesn't matter jack beans. Yeah, but we don't even know the answer truly to that question. And we do know that IRAP's not the only thing that works. So then we're picking one thing out of 300. Oh, but why pick MSCs? No, it's just one of the things, right? It's much sexier. It's much sexier. I'm not asking for you to do an omics analysis on every cell prep. If it has a positive clinical outcome, frankly, I don't care what's in it. Okay, let's get another question because it's all clear now. Go ahead. So with all the discussion of PPP and PRP, is there any consensus on an ideal concentration of the PRP that is optimal? Because each of the products on the market has a different degree of concentration of the platelets. I don't, I would say no. I would respectfully disagree a little bit with tendinopathy. If you look at the data on chronic tendinopathy, the average increase in platelet concentration is about five or five to six on the platelet concentration and does have increased white blood cells. So I'm the dumbest person on the panel here, but I follow the data on does the patient get better or not get better? And if you look at the end point, I think somebody up here, not me, is gonna get a Nobel Prize for figuring out why PRP or BMAC or something else works. But in terms of what patients are after in practical sense, if you're gonna say to somebody, I'm gonna treat you for, as Brian and as Jason said, knee osteoarthritis, the data, the clinical data suggests that leukocyte poor is a better choice. If you're gonna treat tendinopathy and if you're just gonna pick two things, if those two things have reasonable data, you should use leukocyte-rich PRP in a concentration of about five times baseline and with white blood cells. That's it. Our OA data was, our results were independent of our plate. I mean, I can only speak for OA. I have no data on anything other than that, but at least in OA, our outcomes were independent of the fold increase in platelets, whatever that's worth. And I think that's important, and Brian's been doing a great study, which we're all looking forward to, because I think we need to hang our hats on just nuggets that are useful. So when the data comes out on three injections of a lower platelet concentration, leukocyte-poor PRP, then you can be able to say, that's the thing we should absolutely use for knee OA in three injections. And that's where, hopefully, we can move it forward beyond just the people in this room. So actually, I would add to that, which is that platelets have a ton of PDGFBB in them. And I would propose that a simple dipstick test for an ELISA for PDGFBB to tell the doctor like a pregnancy test. If it turns blue, use it. If it doesn't turn blue, take another 50cc draw. Because that, I would propose that with your slide, every company that produces a rig, you gotta give me an outcome of that, because I can take 50ccs for my left arm and 50ccs for my right arm, put them in the same machine, and you'll get a PDGF value that differs by a factor of five. So what does that tell you? It tells you that the number of platelets in the left arm and the right, so my heart's still on my left side, right? So I'm gonna get a different draw. And so therefore, we need the people who make all of these products, these rigs, to give us a dipstick assay that we can correlate with clinical outcome. Because you have no dipstick, you have no assay now to correlate. It's exactly what Brian said. You have no assay to correlate with clinical outcome. So just tell me how much PDGFBB is in the preparation, and then we can design a clinical trial to correlate that with outcome. That's easy. Let's take, I told you we're gonna have more questions than answers, right? That was the first thing I said when we did the introductory remarks. So let's take one more question, and we'll go from there. You were first. Well, how easy is it? That wasn't your question. I said the one over the room. Go ahead, go ahead, ask, go ahead. Yeah. Use the mic, please. If you're getting something rich versus poor, so is that your PR, your platelet's going up to a million five times, and your white blood cell count is going to what? So what's your, and so, and then you're going to do an assay for effectiveness. So what assay does a common orthopedic surgeon have to say, okay, we gave you something that was any good? I mean, it doesn't. I mean, you're not going to do a smear, you're not going to start doing ELISA testing and so forth. You have nothing. You have nothing. Yeah. And you like it. Go ahead. Last one over there and then we're done. So this is just a comment. So one of the challenges with the research on tendinopathies is the same challenge as the variability that we're seeing in the orthobiologics preparations and the challenges in doing studies or comparing apples to apples. So diagnostic ultrasound, the spatial resolution is five to eight times that of MR when it comes to tendinopathy. And so we're learning over time that not all tendinopathies are the same. So latal epicondylosis, patellar tendinopathy, plantar fasciopathy, Achilles tendinopathy, they have identifiable patterns, four or five different patterns that you can theorize would respond to orthobiologics or wouldn't respond to orthobiologics, but we're just lumping all these together. And I think that's one of the challenges when we were looking at orthobiologics and tendinopathies is that we're not comparing apples and apples when we lumped them and that we should try to identify the pathology that would allow us to, in a sense, achieve success. Because I'm not sure it's all just about the orthobiologic preparation, but it's also about the choices we're making with the underlying pathology. All right. Tom Van Ness wants to keep going, but you obviously have nothing to do tonight, right? The conversation is great. I guess I'll say this. We'll go five more minutes, but don't feel like you're being rude if you want to step out, okay? I mean, just stay at it if you wish. Go ahead. So I want to ask the panel two things. One, aside from the subchondral activation with thrombin, do you guys use thrombin any other way for tendinopathy or soft tissue injuries? And two, we talked about doing a series of three PRP injections for OA. Do you do multiple injections for tendinopathy, or do you just do one? Go ahead. I'll just answer the second part, and then I don't want to... So as far as tendinopathy, usually, as long as I use a leukocyte-rich or somewhere around a five times baseline platelet concentration product, usually it's just one, unless there's a significant amount of inner substance tearing, like a rotator cuff tendon, something along those lines. That's most of the time. I'd say at least probably 85% of the time. It takes a little longer for tendinosis to respond than an arthritic knee to a biologic treatment, so you have to tell people to be a little bit more patient. You know, initially, when we first started doing these, we would all say, we'd take two to three and repeat them at six weeks, because you just think about the platelet and the cell biology behind the platelet and the inflammatory and regenerative and proliferative phases, and you would think, that's when I want to hit it again. Well, we got busier and busier. We couldn't get people in, and then we stretched them out to like eight to 12 weeks, and these people were better. So, you know, now we don't even consider it till they're at least 16 weeks out. And most of the time, almost all of them get better, unless they've had like significant tearing or other pathology. For OA, we started with one, and anecdotally, well, our study was with three, so felt good about that, and I would say that I feel good about using multiple injections for OA and have typically used one for tendinopathy. And there's some literature that would actually support multiple, forget about the HA component, just multiple injections of PRP with a progressive improvement for OA. And then for your other question about stabilization with Rombin, right, or activation, I think most people would use it in areas where you have an unstable environment, such as underneath the rotator cuff. It's an aqueous environment. You've done your arthroscopy. You have a lot of saline, so if you then inject it underneath the rotator cuff, is it going to just spurt out? And if you look at Hernigau's data, that's exactly what it does. So then that would be a perfect, maybe, opportunity to use Thrombin to stabilize it in a gel form. Subchondral bone is the same. When you drill in the subchondral bone, it comes right back out just because of the marrow pressure. So to keep it in there, to stabilize it, then that would be another. You know, it's interesting, because intuitively, I would agree. I would say the same thing. A, sometimes this stuff gets hard to clot, even if you use Thrombin, right, to stabilize it. I think it's Rodeo's study looked, I think it was his study, looked at Fibromatrix, right, with cuff repair. And they had a negative, they had an upside-down outcome that wasn't better. So I don't know the answer. It just seems the literature doesn't support our intuition that if you could keep it there longer, it'll do better, you know, the least what's out there. Most of it's in a liquid aqueous format, but the stuff that's looked at otherwise is not really supportive of what we're both thinking. One quick anecdote for that, I'll show you tomorrow morning, but when I first started doing it, I would inject PRP for bilateral epicondylar tendon surgery, and I injected it directly into the extensor tendon in the OR, and I waited, and I waited, and it's somewhere between two and three minutes from the time I injected the PRP, it clotted, and it clots because your tendons are 90% collagen. So if you're injecting it into a tendon and around any collagen, it will clot. So when I inject somebody, I inject them, and then I, if I borrow your elbow for a second, and I just kind of massage it right there, and I hold it for about four or five minutes, because I know it's going to, I first started by doing this and this, and it does flow, but if you keep them level, it's going to be there. For the rotator cuff tendon, it is still unsolved, but I agree with Brian here. It may be better in an unactivated form if you can somehow keep it there. So the PRP? Yeah. Yeah. I mean, the collagen itself will provide that natural matrix for it to, I mean, that natural collagen base. It's a natural activator. Yeah, and it'll actually activate. The reason that I've used it frequently, I'm not a surgeon, so it's kind of, this is kind of a funky trick that we'll do, and in people who have a, not a large, but a, oh, maybe 20 cc or less popliteal cyst, when we're going ahead and treating the joint for Neoway and they have a cyst, I'll aspirate out the popliteal cyst, and I'll combine about a cc of thrombin with a cc of platelet-poor plasma that I've spun a couple times to get that fiber in, and then I, so I aspirate the plate, the actual cyst, the Baker cyst, and I inject the combination. You have to inject it pretty fast, because that kind of fibrin, that fibrin in that platelet-poor plasma with the thrombin will gel pretty fast. You inject it, kind of just hold pressure, and like, those, they do fabulously. As long as you keep the inflammation down in the joint, they don't come back. In fact, my husband's an orthopedic surgeon, and like, he's all, you know, he's a trauma guy, so, you know, whatever, there's the answer right there. But he, you know, he didn't, he's kind of, you know, he had this large popliteal cyst, and I did that, and his hasn't come back in like eight years, and he's like, if you guys did nothing but that, you'd be helping everybody. I'm going to take your last question, if that's okay. Okay, ambulatory practice question. Compared to HA or cortisone, if you're doing PRP or BMAC, do you give any restrictions post-procedure? Do you immobilize? Is it different if you're doing soft tissue versus joint? So why don't we, that's a quick one. I don't do any, I don't do any restrictions with those injections. They may be a little bit sore or so by default, but no, nothing obligatorily. Do you guys do anything? Nothing? All right. No. No crutches, nothing. Okay. You know what? We're going to call it. That's okay. I told you, more questions than answers.

orthobiologics

rotator cuff repair

re-tear

degeneration

tendon healing

platelet-rich plasma

bone marrow concentrate