I have the pleasure of being invited to replace who the NETA Distinguished Scholar Lecture Exchange with AOSSM, A-O-S-S-M, can I say that three times fast? The Foundation Medal for Distinguished Athlete Training Research was awarded to Tamara Valvich-McLoyd, but she was unable to be here, so I'm trying to fill her shoes today. So I'm going to talk a little bit about rotator cuff tendinopathy and talk about how we may monitor the tendon and muscle in particular as we look at defining successful treatment. So the most common treatment that has been studied is resistance exercise, and we can look at trajectory over time, and this is a single cohort of 140 people that we looked at over a course of six months. We can see that they kind of divide themselves into three kind of subgroups, if you will, and we can see that at the bottom on that early, that dark line, people get better and tell us in two different ways that their self-report outcome measures are improving. But they also tell us in the past, if left the way you are today, six months from now would you feel satisfied? And they say yes at a month and six months. And then we have these two other cohorts that have what we call delayed, and then we have a cohort that seems to get better if we just queried them at a month. But when we see them at six months, they're essentially back the way they are. Of course, what I'm most interested in long-term is what are these delayed and unrecovered people like? So our mechanistic model is there's some mechanical overload that exceeds capacity to the tendon. Neuromuscular deficits and tendon structural deficits ensue related to their pain and disability. As you can see on the right-hand side of this slide, there's also a brain attached to the shoulder, if you will. And so there's some altered pain and sensory motor processing evidence that suggests that this relates to their pain and disability, as well as psychological factors. Today in particular, I'm going to just talk about the left part of the equation. So mechanistic theories for tendon. Overload and degeneration I think is clearly now in the largest bucket of what we think is really leading to this tendinopathy. We used to initially think that the compression on the right-hand side in the subacromial space was the primary culprit leading to this rotator cuff tendinopathy. But we now realize that that compression likely doesn't occur as often as we think it may. And I'll talk a little bit about that. But maybe compression between the glenoid that we just heard about, humerus, I'll talk a little bit about that. That may be occurring more frequently than we thought in the past. So can tendon compression occur within the subacromial space? On ultrasound imaging, we can look at this subacromial space and measure the distance between the humeral head and the acromion, understanding what that subacromial space may look like. And this is a linear measure, not a three-volume metric measure of the subacromial space. We can see from other imaging techniques, in cadaveric studies we can see that the compression can occur in that subacromial space. When we start doing some modeling studies, we can see that the smallest subacromial space is really in that 0-60 degrees of elevation. So the space which the red represents, the tendon, and the space is between the humeral head and acromion, 0-60 degree elevation is the smallest space. Once we get past about 70 degrees, as you can see on the right, the tendon footprint is no longer available for compression. So if compression is occurring in the subacromial space, it's below 70 degrees. So if somebody is complaining of pain up here, it can't be compression. It's not available for compression. But you are loading the tendon, so loading is likely this reason, potentially, that they may be having pain. Other structures as well, but just concentrating on the tendon here. So if the subacromial compression does occur, it's in these lower angles. This posterior superior impringement, we can also see through two mechanistic studies that I'll just talk about. In ultrasound we can see dynamically that the tendon can become impinged in this posterior superior. And we think about what we just heard a lot in this thrower population. But this might be occurring also in the non-throwing population. We look at the tendon footprint and the glenoid contact in these same modeling studies that we talked about on the last slide. We can see that compression can be occurring where the footprint is at about 125 degrees of flexion and scaption elevation. So in this reaching overhead kind of position that this compression can be occurring. And this is in non-throwers. So technically when we think about this, this is likely also one of our culprits. So what should we call this? It seems like subacromial impingement is not a great label because there's more mechanisms. Shoulder pain, my personal preferences, that seems so vague. And also, why not just call it rotator cuff? But that is one option. Is it tendinopathy? Do we know that the tendon is truly always the culprit? And subacromial pain syndrome implies subacromial space only. I don't know which one. I just know that subacromial impingement is probably not the one to be calling it given that there is multiple mechanisms. So how might we measure tendon and what do we know about this? This is in a longitudinal view of the tendon. And we know in people with painful rotator cuff, there's been multiple studies. The tendon is thicker by about 1.3 millimeters. That range goes from .6 to 2 millimeters depending on the study that we're looking at. And that's compared to their unaffected shoulder or healthy controls. The problem with tendon thickness as a single measure is if we look at baseball players, I have a whole other group of research that I look at baseball players. Ironically that would have been the good talk for the overhead throwing talk today. The thickness is also thicker in baseball players on the dominant side. So does that mean they're unhealthy, that tendon, because they're thicker? If we look a little bit at a different measure to understand what's happening, the micromorphology within the tendon, we can take the same ultrasound measure and we can do some 2D transform and look and understand these brighter, which we believe to be the collagen, that we can end up being able to boil this down, if you will, to this single image and then measure the peak spatial frequency radius between these two bright bands, if you will. This peak spatial frequency radius infers disorganization of the collagen. We know this from a master study that was just recently published that they actually did ultrasound, did some micromorphology, punched biopsy the tendon, looked at histology of the tendon and demonstrated that in this altered peak spatial frequency, if it's lower, it does indicate less organized collagen. So this coupled with tendon thickness might give us a better idea of what's happening within the tendon. The tendon's thicker, but it's also disorganized. We also know there's some altered neuromuscular performance, muscle activity, or onset of muscle activity as the elevation, also ratio between the scapular muscles as well as the cuff muscles and other related shoulder muscles may also be a culprit. And they're somewhat related to scapular kinematics, but unfortunately, they're highly variable related to scapular kinematics. So if we just look at the muscle, we can potentially understand the importance of the muscle as loading the tendon for tendon healing or reorganization of the collagen. And so right now, just from a pilot, I'll talk a little bit about this result. We're looking at tendon prior to the onset of a resisted exercise program. We're looking at both thickness and this micromorphology as well as some self-report outcome measures. At this point, I'll just talk about the two-week outcomes. We're defining people who may be considered responders by looking at a conditional SEM based upon their baseline scores. Are they improving or not over this meaningful amount? We also ask in that pass that I inferred about before, if left the way you are today and six months from now, would you consider your status acceptable? We're trying to triangulate what we think likely represents a responder. What we see is that in this responder group represented by the blue, pre-interventions on the X-axis on the left and on the right is the post-intervention. So this is over time. And the Y-axis is tendon thickness. We see the responders are thicker to start with and they tend to get closer to what healthy match controls are in black. Interestingly the non-responders, people who don't respond as well in that first two weeks don't seem to have that much of an issue with tendon thickness. And they don't really look different after two weeks. When we looked at micromorphology, the story is a bit different, hence I think arguing for a more multidirectional view of this. And responders look a little bit different than non-responders in this micromorphology. Rate of force development and peak force are things that also people would like to use to look at muscle. Using the same setup, what we see is that peak force improves a bit. This is pre-intervention and post-intervention, peak force improves a bit. But what really seems to separate is how fast they can generate that force. And what to do? Looking at muscle performance in tendon response and looking at understanding who's responding and not. Thank you.

rotator cuff tendinopathy

resistance exercise

cohort study

mechanistic model of tendinopathy

tendon compression