Perfect. All right. So now we're going to move on to osteochondrosis. So this is another one where we know quite a bit about the pathophysiology. it's pretty complex. So I'm going to do my best. But if you have any questions I'll try and come back and answer those and I can come back to pictures and things at the end as well. So the little blurb that you will find whenever you read anything about osteochondrosis is that it occurs as a result of a disruption of endochondral ossification. That's the sound bite. So what does that mean? It means, unfortunately, that we have to talk a little bit about how bones actually grow and develop, which is a complicated process, but we'll do our best. So essentially our long bones are going to develop from a cartilaginous blueprint. So basically there is cartilage that is produced to create the shape of the adult bone. And then over time, as the animal matures, that cartilage is gradually replaced with bone. So there are two main places where that new cartilage that is eventually going to ossify and turn into that new bone, where that new bone is being produced. One, of course, is the physis. Believe it or not, even though the physis is the main location where bone lengthening is occurring, it's not common for us to see osteochondrosis lesions affecting that. Couldn't really tell you why. You know, they probably occur but are subclinical in most of these cases. So we're actually going to kind of forget about the physis and we're going to focus on the other place where new bone is forming, which is the epiphyseal plate. So I've got a picture here, that shows all the way over on the left, this is a very, very young animals epiphysis. So this is the basically the cap of this animal's long bone that is being evaluated histologically. And so, the majority of this light pink material that you see right here is cartilage. And then in the center the darker pink that you see is new bone developing. So this is the epiphyseal ossification center at the tip of this animal's long bone. So initially in this young animal there's been minimal new bone formation. Mostly we are still dealing with the cartilaginous blueprint. So look how thick this layer of cartilage is. Super, super thick. Over time, this ossification center in the middle is going to spread outward. And so if we then look at this second picture, you can see how more and more new bone is beginning to form. And so it's gradually spreading outward. And if you compare now we have much thinner cartilage left behind. So all of this was cartilage before. Now only, you know, maybe a quarter of what was present before is still cartilage. The rest is being turned into bone via this process of endochondral ossification. And then finally, as we get, you know, closer and closer to skeletal maturity, this ossification center is eventually going to, almost completely fill the epiphysis such that we only have that thin layer of cartilage left behind that will eventually become our articular cartilage. Okay. So in the adult, remember, the caps of our long bones are covered with a thin layer of articular, hyaline articular cartilage. And so that again is going to provide that nice smooth surface to allow frictionless, weight bearing. Obviously it's not completely frictionless, but you know what I mean. It's going to allow that, that smooth, range of motion during weight bearing. Okay? So we should have just this thin little layer of articular cartilage left in the adult. Okay? So important to recognize, again, when we're talking about the epiphyseal plate in the process of endochondral ossification at the epiphyseal plate, this is the bone that is eventually going to form our subchondral bone. So this is the bone that will be right up against the joint surface. And so lesions that affect this developing epiphyseal plate and potentially and do produce lesions that affect the joints. I think that's probably why we see much more issue with oseteocondrosis here because joint disease is something we can recognize easily versus lesions that affect the physis. I think A have probably a better chance of being able to resolve on their own, and B may have less clinical significance. So when we're talking about osteochondrosis, we're primarily worrying about lesions that affect this epiphyseal plate. Okay. 

So, again, if we are, develop, if we are developing, our subchondral bone, this is an example of, an adult, and so we just should have this, relatively thin layer of articular cartilage that underneath is supported by nice sturdy bone that's subchondral bone. And so as this epiphyseal plate is growing outward, what we can see is that if a lesion comes along, any lesion and we don't know exactly, you know, what occurs, you know, might be a traumatic lesion, it might have something to do with some sort of, hypercoagulable event, you know, maybe there's some sort of nutritional thing or some sort of genetic issue with, adequate blood supply in this region. But in order to grow and to heal, bone has to be supplied with blood. And so if an area of this, articular cartilage becomes necrotic, for whatever reason, if this if an area becomes necrotic, it can potentially create a barrier beyond which ossification cannot progress. And so instead of just having this, you know, kind of normal thin articular cartilage left behind, we might actually end up with a focal area where it is much, much thicker than it should be. Because ossification has not been able to progress as normal. Okay? If this is only a very small lesion, this might be something that could resolve on its own. In which case that would be termed an osteochondrosis laten's lesion. We know that these occur, but they're not clinically significant because they are not present in the adult. This is something that can heal on its own essentially. So, you know, take osteochondrosis latens and just throw it out of your brain. You've got so many more important things to put in there instead. It's not clinically significant. Don't worry about it. I just included it to be complete because you'll see it whenever you look at diagrams and things for this disease process. Okay. So forget about osteochondrosis latens. We don't care about that. It's not clinically significant. We care a little bit more about osteochondrosis manifesta lesions. In those cases, the osteochondrosis lesion, the area of maybe necrotic cartilage that has formed a barrier to, new bone formation, it's big enough that it cannot resolve spontaneously. And so essentially what we end up with in those animals is an area where that subchondral bone does not develop, does not form. And so instead we just have this thickened plug of cartilage much thicker than it should be. And so you can see that on radiographs. So I'll go back to my first picture. So you see how it kind of looks like someone took an ice cream scoop and just took a scoop out of this dog's humeral head. That's what osteochondrosis looks like. It's not that there's nothing here. But what is here is only cartilage. It's not filled in with bone like it should be. And so we have this focal subchondral bone defect. Does this matter? Immediately, no, because again, it's not like there's actually a defect there. You know, the animals joint surface is intact. It's just that focally there's an area where that articular cartilage is much thicker than it should be. But the problem is that cartilage is not as strong as bone. 

And so over time, what we can see is that that area of thickened articular cartilage, where we're asking the cartilage to do the work of bone, cartilage just can't do that forever. And so what we can see is that that area, that defect can develop little cracks. You know, there's still cracks that can run down through the abnormal thickened cartilage, little fissures that can get all the way down to that underlying subchondral bone. Sometimes that area of thickened cartilage cracks off entirely and actually lifts away from the underlying subchondral bone. And so those things are bad because now we do have a defect in our joint surface. We have exposed subchondral bone that causes a lot of inflammation. And so at that point we no longer have an osteochondrosis manifesta lesion, we now since we're dealing with inflammation we're dealing with pain, now we have a clinical osteochondritis lesion. So this is usually when we identify these cases in small animals. You know if you went out there and you radiograph a bunch of golden retrievers, you would probably find some osteochondrosis manifesta lesions. So, the animals not clinical for. But most of the time when we're picking up on these, it's because the animal is clinical. And very often that indicates that they have moved on from an osteochonrosis manifesta lesion, that area of abnormal thickened cartilage has started to break down under pressure. And we have actually reached the point where now we have an osteochondritis desicans lesion. Okay? So if you look at this image here, once again, you can appreciate that there is an enormous subchondral bone defect. So this is the normal, surface of the, the subchondral bone. And you can see when we get to about right here how it gets irregular, like this is a huge lesion and then lifted off adjacent to it, you see this little line of mineralization. You might be like, wait a minute, I thought we couldn't see cartilage on radiographs. Very often in these cases, as a result of chronic inflammation, we see dystropic mineralization of these cartilage flaps. So this is actually just a mineralized flap of cartilage that has lifted away from the surface of this animal's humeral head. So that's when we expect them to come in be radiographed, be clinical. Hopefully that made sense, like I said, if you have any OCD, pathophys questions, feel free to toss those in and I will try to go back and clarify. 

Otherwise, generally when we identify these lesions, we tend to see that our large and giant breed dogs are once again the ones that are predisposed. They will often present with either a unilateral or a bilateral lameness, pain, diffusion, crepitus, all of the signs that there is a problem with the joint, in whichever limbs are affected. We're going to get to the predisposed sites in a second. But in general, we expect to see signs of, joint pain, joint disease, associated with wherever the OCD lesion is. It is important to recognize that a lot of these dogs will be bilaterally affected, even if they are not equally clinical on both sides. And so it is strongly recommended that if you identify an OCD lesion in one limb to radiograph the contralateral limb as well, because, you know, you might find, oh yeah, he's painful in this shoulder because he has an OCD lesion over here. But if I radiograph guess what radiographically he also has maybe an an osteochondrosis manifesta lesion. Maybe he's not clinical for it yet, but there is a lesion on the opposite side as well. 

Diagnosis again, like we've been talking about. You'll identify these focal subchondral bone defects. Sometimes with a, mineralized flap, either adjacent to them, like in the picture that we looked at a second ago, or sometimes, sometimes that flap actually breaks off, and then it can go somewhere else in the joint capsule. So if you look at this radiograph you can see this again little linear section of mineralization. That's actually a little cartilage flap that has broken off and disappeared into the depths of the joint capsule. so that can be a problem too, because sometimes those, little flaps go somewhere where they shouldn't like underneath, for example, the biceps tendon. And we can see things like secondary biceps tenosynovitis because of that migrating little flap. Other times they go into the recesses of the joint capsule and may not cause a huge issue. But in all cases, we're looking for that subchondral bone defect. I'll have more pictures and a little bit of some other locations, but I know I've got a whole bunch of pictures of the humerus here, just because it's such a nice joint to look at. Such a nice example. But especially in elbow dysplasia. I'll show you some other pictures of, other OCD sites, but they all look similarly again. I just imagined it as someone taking an ice cream scoop and just like scooping out a chunk of that subchondral bone. And so, again, we know that unless the flap has broken off and gone away, you know, there should be a, area of thickened cartilage present here. It's not that there's nothing here or a defect in the joint surface. In an OC manifesta lesion, that joint surface is intact. It's just that the cartilage is thicker than it should be. Only, only after that cartilage flap has gone away do we have that defect in the joint surface. That then tends to cause a lot more clinical signs. So again, looking for that focal subchondral bone defect, especially in other joints like tarsus, elbow. The lesion may not be as obvious on plain films as it is for like, the humeral head. And so those cases may benefit from CT. Again, we do tend to identify OCD lesions in very predictable locations. The four big players that I think are important to know about our the caudal humeral head, the medial humeral condyle, the lateral or less commonly medial femporal condyle, and the medial or less commonly lateral trochlear, trochlear ridge of the talus. Those are the four big locations in small animals. Large animals are different, but in small animals, those are the four, like big players in OCD. So especially if we have a young large breed dog who comes in with signs that are localized to one or sometimes more of those classic locations, that's a big thing that we want to be looking for on our imaging. And even if we can't see it, if we're strongly suspicious again, remember that CT may be more sensitive in those cases. 

So once we've identified these lesions, especially for the symptomatic dogs, you know, the OCD dogs, we do generally recommend surgical treatment. There's two big options surgically. The first options are considered the palliative techniques. And then the second options are the joint resurfacing techniques. So for the palliative techniques the idea is that we go in either arthroscopically, which is nice because then we can see better. We can look around the whole joint, we have better access, or via an arthrotomy. So we make an approach to the joint and then we remove that area of damaged abnormal cartilage. So if there's a loose flap wiggling around, we grab it, we pull it out. We debride any unhealthy malacic softened articular cartilage. And we debride the underlying subchondral bone, with the idea that we can get it bleeding because a lot of times underneath the flap, the subchondral bone is, very sclerotic, very dense. And so it's not bleeding very much. And we actually do want to get it bleeding, because that's going to help to stimulate the animal to create fibrocartilage in that area instead. Fibrocartilage is definitely not as nice as hyalin cartilage as a joint surface, but it's better than having soft malacic abnormal cartilage, or a loose, unstable flap. And so, the idea again, is that we are just trying to debride any overtly unhealthy articular cartilage so that the animal can then form fibrocartilage in that area, to help cover that joint surface and improve their clinical signs. However, like I said, it's not the same as if this had never happened. It's not as good as having actual hyaline cartilage filling that defect, especially if you have a really big defect. That joint surface is still fairly abnormal. And so, while we can generally make them more comfortable with the palliative techniques, at least initially, progressive osteoarthritis is going to be a feature, for those dogs and especially for large lesions, especially for complex joints like the elbow or the tarsus. Progressive osteoarthritis can be a big limiting factor for how good their long term outcome actually is. Because again, if that joint surface is disturbed, that leads to significant arthritis, degenerative changes, loss of range of motion, chronic pain, and so in some joints that is better tolerated than in others. So at the end of this I have a little chart where we'll talk about the different sites individually. But definitely there are some joints that are less forgiving of those progressive degenerative changes than others. Where treatment of OCD lesions can be associated with, you know, just not as great outcomes. More experimentally, there are joint resurfacing options that have been described. In some cases, the use of a an osteochondral plug. So basically going to usually the stifle, and harvesting a non articular section of bone that also has a little cap of articular cartilage, and then coming back to the affected joint and implanting that osteochondral plug, with the idea that then that that will heal in place in the animal will have a more normal joint surface. That's called the OTE system. So that's been described. And then there are also synthetic implants that can be used to try and fill these lesions. Again, the idea is just that this is going to produce a somewhat more normal surface to the joint. So that we don't have that fibrocartilage filled defect present anymore. Hopefully that can result in slower progression of osteoarthritis relative to the palliative techniques. But again, this is still not a situation where we can make the joint completely normal, and management of degenerative joint disease is going to remain important. Usually the joint resurfacing techniques are described more for the, the, femur and the shoulder. A little bit less commonly for some of the other lesions. Just because of the complexity of the anatomy in those joints. 

So like I said, there are some kind of differences between the, the locations. So shoulder, elbow, stifle passes are four joints that are most affected for OCD lesions. In general, if you're going to get an OCD lesion, get one in the shoulder. This joint, I think it's I think I think it's honestly more reflective of the anatomy of the shoulder joint. You know, it's a big, wide, relatively flat joint that has this wide surface for articulation. It's a joint that is very tolerant of degenerative changes. You know, you'll take a radiograph of an animal, you know, an older animal, and you'll see that it has really pretty marked shoulder arthritis. And the animal is fairly pain free. You know, moving around doing normal dog things like life is good. So I think honestly that it's just that the shoulder is very tolerant of to or dogs are very tolerant of degenerative change in the shoulder as a result of having that like really nice flat, tolerant, joint surface. The elbow and the tarsus on the other hand, are a lot less, tolerant of degenerate changes in my experience. And so, I do worry a little bit more about prognosis in those guys, especially with large lesions. We worry about it. Same thing with the stifle. We see a lot of stifle disease in general in dogs. And, these tend to be fairly large lesions as well. And so, we tend to see a little bit poorer prognosis with those locations as compared to the shoulder. Shoulder is the one that you want to have if you're going to have an OCD lesion. Although OA, or sorry, OCD, one thing that I do think is important is to recognize that it's usually in combination with other components of elbow dysplasia. So we're actually going to talk about it again in a little bit. And then just knowing that stifle and tarsus tend to have the poorest outcomes for osteochondrosis. The good news with Tarsus is that tarsal arthrodesis can be a very good salvage option. Stifle in some ways is hardest to deal with. And that does tend to be why we might push a little more for the joint resurfacing techniques in that location as compared to, some of the other locations, because, again, the tarsus tends to, just not have the outcomes that we would like and tends to have fairly large lesions noted there. All right.