I think some individuals have some flights to make, so there's really just a couple of points that come out here. I might even skip a few slides because I think we can make the point. If you're in this room, you know the rotator cuff repair is an important problem, so let's just kind of move ahead here. But here's where we are. We know that tendon healing is a slow and certainly imperfect process. There are both biological and biomechanical challenges. I'm going to sort of set the stage with sort of the clinical problem here. And in doing so, consider both clinical outcomes versus structural outcomes. Clinical outcomes, again, are those measured by standard patient-reported outcome measures. Generally, you can improve pain, whereas improvement in strength is less predictable. Structural outcomes is this issue of does the tendon heal? And when you'll see the term re-tear, I kind of prefer to say failed healing. I think it's more accurate. I think these tears never really healed in the first place. That's what we're going to explore today. So wide range of reported failure in the literature, up to 94%. All techniques, all tendons, no matter how you evaluate these, these are the numbers that you're all familiar with. Probably more realistic numbers are kind of 15 to 20% of failures with contemporary techniques. But this is the study from the Washington University, Lisa Glatz and Kenyem Gucci, people often quote. And this is sort of an earlier study, 2004, single row repair. But this is the small group of patients where they had this high failure rate, 17 out of 18 by structural evaluation with ultrasound or MRI here. But the majority of these patients, like a lot of studies, actually did pretty well. They had pretty good ASES scores, they get pretty good motion back. Certainly though, these kind of results did deteriorate over time. This might've been due to a lot of factors. Early days of arthroscopic repair, single row repair, fairly aggressive rehab with early pulleys, which are probably not so passive. So that may be some reasons. More contemporary data. I want to put one, use one recent study just published this year that really summarizes things well, a systematic review that went through the effect of double row, PRP, and effects of early motion. And we'll kind of evaluate these three things on the healing rate. So if you compare double row versus single row, what is our failure rates? Double row repair, you see the numbers here, single row a little bit higher. The majority of studies showed a lower re-tear rate in double row repair. On the clinical side, a couple studies show some improvement with the double row repair, but really generally pretty similar outcomes clinically. But a higher failure rate with single row repair, this is just the data from their paper. I would encourage you to look at this paper. It's recently published and it has all of this data. The second thing they looked at is does PRP make a difference since this is so topical and you're going to talk about biology here, I thought I'd put this in. Structural outcomes with PRP, you see the numbers there, no PRP. It seemed to be a lower re-tear rate using pure PRP for small to medium tears. There's some decent, well done studies that demonstrate that. In contrast, a platelet-rich fibromatrix is not effective. Clinical scores, very little difference there. And again, no effect for platelet-rich fibromatrix. So you do see some effect for PRP with small to medium tears. And this is the data, this is just redundant from their paper. And lastly, they looked at motion, early motion versus late motion. Early motion, you see the numbers here, late motion, no difference in re-tear rates or failed healing rates. Earlier motion group had better motion, as you'd expect, at the early time points. No difference in the clinical outcomes, and there's the data there. So structural outcomes generally do not correlate with the clinical outcomes. Patient with quote-unquote re-tears often have good satisfaction. At the same time, we have patients that have an apparently healed repair that may have persistent symptoms. We clearly need more discriminating patient-reported outcome measures. But at the same time, failed healing or re-tear certainly is relevant in our younger patients where more active patients will note, they will note the weakness and not be happy with their outcome in those settings with the re-tear. But there is this sort of disconnect between structural and clinical outcomes. An important study that kind of looked at this is Jess McCarran from Cleveland Clinic. They measured tendon retraction after cuff repair. They put little metal beads, tantalum beads, in the tendon, as you see in the picture here. They did a CT scan at serial time points up to a year and looked at the 3D position of the beads in the bone and the tendons. You could look at retraction. They also used MR to assess for recurrent tendon defects. And their data is interesting. All repairs retract from their final position over that first year, an average of about 16 millimeters. And whether or not the patient developed a quote-unquote defect or a failure on MR, no difference in the amount of retraction. Average 16 millimeters. In fact, only 4 out of the 13 patients formed a recurrent defect, whereas they all had some degree of retraction. They coined this term failure in continuity, where you see tissue, you know, connecting from A to B, but that tendon has retracted. You see the muscle tendon junction is medial. Those patients who formed a recurrent defect did have more tendon retraction during the early time period. And keep that in mind. It points out the importance of protecting our repairs early. On MR, you can see there's a correlation between the amount of bead motion and the degree of medial retraction of the muscle tendon junction. You could use your MR to kind of get a sense, obviously, of retraction there. No real correlation between the magnitude of retraction and some of the outcome scores. But this data suggests that absence of a recurrent tendon defect on either MR or ultrasound may not be sufficient to conclude that the tendon has healed at the site of fixation. And it's an important kind of conclusion. We've seen the same thing in our animal models. You do a sheep repair. Here's our tissue. Often, you look at these grossly, it looks like you've got an intact repair. MR clearly shows the same thing to this retraction here. Time unit of failure. Most of these occur in the first 12 weeks after surgery. Another radiostereometric study. This is just 10 patients, but again, putting metal beads in the tendon and the bone there. Repaired cuffs retract immediately at about 8 millimeters during the first year. So you can see, same type of thing. Largest increase kind of happens in that first kind of 14 to 16 weeks. More than half of these patients had a defect. So you see this retraction, but they don't all have what you'd call a defect. There is more marker movement, more retraction in those who were failed or retorn. Time unit of failure. We had looked at a similar thing, Joe Iannotti and myself and some others, in a multi-center study. And the salient points here are we had a 17% failure rate in this group of 113 repairs. Linear increase in re-tears over the first 26 weeks. So you see on this graph here, most all re-tears occur in that first half a year, by about 6 months. So re-tears primarily occur between 6 and 26 weeks. Bruce Miller had a similar study, I'll skip this in the interest of time because it really shows the same thing. Their graph here, if you just look at their re-tears, 200 days, that's 6 months. So most of these occur after the 6th. So I think the implications here are most failures occur by 6 months. Many occur between 6 and 12 weeks when you initiate active motion. So we need methods to protect the healing tendon in that early post-operative phase to allow structural healing during this vulnerable time. And that's what some of the later speakers will get to, how we can augment the biology to do that. Age. We know the failure rate increases with age. A number of studies kind of demonstrate this. This study probably here is the best to kind of make the point from George Morrell. 1,600 cuff repairs and you see the re-tear rate according to patient age here just goes right up. Just a linear increase by decade. And you see the same thing if you stratify by small, medium, large tears. Same pattern. So obviously age is the factor. Other important factors, these are factors we can't really control. Some are intrinsic to the tendon. So the tear size, the degree of retraction, fatty infiltration, all these have an adverse effect on healing. And then patient factors, diabetes, hypercholesterolemia, obesity, and maybe other metabolic conditions that affect tendon biology, genetics may play a role as well. Why does this occur? And this will kind of set up for the remaining speakers here. I think the bottom line is failure to re-establish the structure and composition of the native enthesis. You know, we take a tendon, we do this, we repair it, we'd like to have this happen, a native enthesis. Well, in fact, we get this, this fibrovascular reactive scar formation. You know, why does this occur? I think it's due to absence or deficiency of responding cell population. There may be absence of appropriate signaling molecules to direct tissue repair. Maybe the inflammatory response and inflammatory media probably plays a role, as does mechanical loading. All of these factors here, these four I would submit to you, are important to consider in thinking about the biology of healing. So the question for us is, will biologic augmentation approaches improve cuff healing? And that should lead to the next speakers here. Thanks.

rotator cuff repair

failure rate

platelet-rich plasma

early motion

biologic augmentation