Hello everyone, welcome to another one of our webinars. This time we're gonna be talking about a surgeon's approach to the management of degenerative joint issues, and this webinar has been kindly sponsored by Protein, so thank you so much to Protein, and I'm really thrilled to have Doctor David Dycus, who's going to be speaking to us today, based at the Nexus Veterinary Bone and Joint Centre in Baltimore. David attended the Mississippi University, first of all, and graduated with his veterinary degree, and then did a small animal internship at Auburn, and then went back to Mississippi State to do a residency in surgery and a master's degree.

He's lectured extensively across the world and has given over 200 continuing education lectures. He's also the author of several book chapters and the co-editor of the textbook Complications in Canine Cranial Cruciate ligament Surgery. Obviously a condition that we see very, very regularly.

As well as this, David is a, is on the board of trustees, the American College of Veterinary Surgeons and is a council member for the Association for Veterinary orthopaedic Research and Education. David is also very interested in canine rehabilitation. He did a course with them through the famous University of Tennessee's rehabilitation course.

And really excited to, to see what David's thoughts are for what is an incredibly common condition. So over to you, David. Thanks so much for the, the great introduction.

I am thrilled to be able to join you all this, this evening for me. It's, it's early afternoon, so just getting, getting home from work. And so I certainly appreciate you joining in, taking your, your evening time to hopefully learn more about how I as a surgeon, approach the management of degenerative joint issues.

And so, I am going to go ahead and stop my video, so that way you don't get too focused on looking at me, and we can focus on the presentation and then at the end, I'll turn the video back on and, and hopefully, we can have some lively discussion on, questions and answers. So, just as we get started, Give me just a moment, having a, just a little bit of a technical. Difficulty here.

Let me see if I can get this to, to fix really quickly. I'm sorry. OK.

So as we get started, just a few disclosures to go through. I do lecture and consult and do research for a number of companies that are mainly located within the United States and, and some of them have reaches abroad as well. So if you happen to see images of particular products, it doesn't correlate to any personal or company preference.

So as we get ready to start, again, sorry, I'm having some some technical difficulties here. Let me, See if I can get this back appropriately for you. So to get started, you know, when we start thinking about the management of, of osteoarthritis, I'm gonna show you two radiographs here and, and ask a question of do these patients need the, the same type of, of management.

So, the image in the upper left portion of the screen is gonna be a dog with pretty severe elbow osteoarthritis versus the one in the lower part of the screen. It has what I would consider mild elbow osteoarthritis. And so we want to ask ourselves if these patients need the same type of management.

They have the same, disease condition, but a different severity, and they also have the same disease condition within the same joints. Another way to look at this is looking at this slide and asking ourselves if these patients need the same type of management. So the radiograph on the left is going to be a patient with stifle fusion and osteoarthritis of the stifle versus our patient on the right has a pretty severe bilateral hip osteoarthritis.

And so now, we have the same disease process, but it's in a different joint. And I think one of the things to think about with me showing you radiographs is, is that all of the story when we're looking at patients with, with osteoarthritis and how we might make our approach to management for these. And so, what I'm hoping that you're able to take away from this presentation is first and foremost to recognise that osteoarthritis affects the entire joint.

And I want you to appreciate Oh goodness. David, would you like to try and take over the slides and forward them for you? Actually, what I might do is, is let me just do this, and this is gonna be the backup plan that should, should work, so I apologise for, for that.

David, while you're doing, just ask people if they wanted to to tell us where they're listening in from in the chat. So if you do want to put us in chat, we've got somebody listening in from Romania, so it's great to see people listening in from, from all over the world. Absolutely.

Thank, thank you so much. And, and, ultimately, I had to change over my, my viewing inside. So, you know, I should, I should remember all my slides.

So, you know, the second thing I want you to take away from this is, is to really appreciate the ebb and flow of, of osteoarthritis, meaning where we have these periods of calmness followed by periods of flare-ups and, and what exactly that, that really means. And then lastly, appreciate the multimodal management. And we'll start by defining some of the goals we want to achieve with the management strategy and then how we might achieve those goals on various aspects of, of management.

And so, if we look at what osteoarthritis is, there's a really nice academic definition, but if we break it down to very simple components, It's basically the gradual loss of articular cartilage, which is going to lead to failure of the joint. And so our job needs to be to recognise the disease condition. And then from there, try to institute principles to minimise the getting to the point of the joint failing, or at least provide appropriate quality of life so that patients are comfortable such that when the joint does fail, they are older, or we have other options available to us such as joint replacement or joint fusion.

So, osteoarthritis is the most common form of, of arthritis in dogs and cats. It's more common than septic arthritis. It's more common than our immune-mediated arthropathies.

And it's been said that about 20% of adult dogs and about 60% of adult cats have radiographic evidence of, of osteoarthritis. But what's important to remember here is that radiographic signs don't always correlate to clinical signs. So think about when you've had the patient that comes in for acute vomiting and diarrhoea and you take radiographs of the abdomen and you happen to catch the hips in the radiograph and the hips look really, really bad.

But the dog's never had any clinical issues associated with the hips. So does that mean we now send the dog to the surgeon for a hip replacement, or should we ignore it because the dog's not having a problem? And then owners themselves are also getting very smart as far as osteoarthritis goes.

And in fact, with the advent of things like the internet, 31% of owners have said that bone and joint problems were an issue with, with their pets. And so, what I would say is, at least with my clientele, my clients tend to be members of various Facebook groups and email chains, and, and so I walk into an exam room and they're sitting there with a big manila envelope full of, of files and information they've found, and they've armed themselves with education. And it sometimes hits home when I start talking about the management of osteoarthritis because what's happening is a lot of the same management strategies we discuss with owners for their pets.

If they themselves have osteoarthritis, it's some of the exact same management strategies so that they can actually start to relate to what we're trying to achieve. And so, at least in the United States, osteoarthritis is the number one cause of chronic pain in dogs, and it actually has this sort of vicious downward spiral of cascade of events where if we have a patient that has arthritic changes. Either the owner doesn't want to cause pain to their pet or the dog's gonna self-limit.

And so there's a decrease in activity, which then means that there's over time going to be a loss of range of motion because the joints not being used appropriately. But at the same time, if the dog is still eating the same amount, they're going to put on weight, which is going to further compound the issue, and there's going to be an overall negative impact on the patient, which can interfere with the human-animal bond. And in some cases, if we have dogs that are non-responsive to management strategies, then sometimes quality of life gets affected and we start thinking about would euthanasia be a solution to relieve this pet of the discomfort they're having.

So we want to think of osteoarthritis or OA as a global disease process. So we don't want to think about it as an isolated disease entity and, and remember that it's the final pathway of the failing joint. But what I want you to start thinking about is thinking of the joint like an organ.

So, for example, We take the stomach. Well, the stomach has a number of different cell populations and layers that all collectively work together for the stomach to function as it's supposed to as an organ. Well, the joint is the exact same thing.

There are a number of tissues. For example, the joint capsule, the subchondral bone, the periarticular tissues. All of these have Crosstalk amongst themselves and all of them have aspects that are involved in joint function as well as the repercussions of osteoarthritis.

And so while we think about the articular cartilage, mainly as the component to OA, what we really want to think about is there are other structures involved and we don't want to forget about those. And so when the dog, It's almost always a secondary issue, meaning we should ask ourselves, what's the primary problem that's causing this dog to have arthritic changes? Meaning is there a torn cranial cruciate ligament or does this dog have developmental elbow disease or hip dysplasia, or a medial or lateral patella luxation?

Cats are a little different. And that we tend to see more primary osteoarthritis, and it tends to be idiopathic in nature and it and it goes down a little more of an avenue. To some of the aspects on the human side where we can have the development of osteoarthritis to form from not having necessarily a primary problem.

So let's look at the joint. The image on the left is a normal joint and the image on the right is an arthritic joint. So what are some things that we, that we might see?

Well, we can see a thickened joint capsule. Over time, there's going to be joint effusion, which is gonna put capsular distension in play, and the capsule is gonna respond by getting thicker over time. It's Also going to be associated with perarticular fibrosis surrounding it.

And the joint capsule itself has a very rich, robust blood supply and innervation to it. So think about if you're going into the operating theatre for a dog with a ruptured cruciate ligament and you make an incision in the joint capsule. Number one, it's, when it's thicken, it'll sometimes bleed a lot.

But number 2, Every now and then you may notice as you get close to the joint capsule, the heart rate in these patients will start to go up because it, it's got a very rich nervous supply to it and, and so they can appreciate noxia stimuli from this. What I consider the forgotten child when it comes to osteoarthritis is the synovium, because the synovium is responsible for the production of nutrients to the articular cartilage, but also it's what's driving the inflammatory response. A lot of those inflammatory mediators and derogative enzymes are being released from the synovium.

And then there's also an impaired exchange of nutrients and waste, from inside to outside the joint when the synovium is inflamed. Of course, we talk a lot about the articular cartilage and it really has a simple function. It's, it's job is to dampen the compressive forces onto the joint and, and transmit that, to lower the compressive forces onto the subchondral bone.

It's important to remember that the articular cartilage is avascular, so it has no blood supply. It's a neural, so it has no nervous, tissue to it. So, pain associated with osteoarthritis doesn't come from the articular cartilage.

It's coming from these other structures. And because it's avascular, it has to get its nutrients through diffusion in the joint fluid, and those nutrients are typically coming from the synovium. And so you can see how all these portions are intertwined and work together.

To cause the global disease process of, of osteoarthritis. And then over time, we'll start to see thickened subchondral bone because it's trying to adapt to different biomechanical forces being placed upon it because the articular cartilage is not functioning appropriately. And so when I think about the pathophysiology of osteoarthritis, I really think about this ebb and flow scenario.

So think about the sea, for example, the tide comes in. The tide comes out, we can have very nice, beautiful days at the water, and we can have these really bad, rainy, stormy days. So what the heck do I mean by this?

Well, we can characterise the flow of osteoarthritis somewhat similar to what they do in the person where we can have these periods of calmness or, or remission. This is a nice day on the beach. Life is great.

We're enjoying the weather, Things nice. We know that our patients have a way, but they're not clinically affected at that time. So our management strategy here is gonna be to focus on what I call the baseline.

And what that means, we can talk about things like joint supplements, our omega 3 fatty acids, our disease modifying OA agents. We also need to put a very big focus on Weight reduction, maintenance of strength and, and development of fitness, as well as what the heck is this concept of daily exercise. The opposite of this would be our flare-ups or periods of exacerbation.

The day on the beach, this is no fun anymore. We want to retreat. We want to get out of the storm.

We know they've got osteoarthritis, and they are clinically affected at the moment. So, our management strategy really needs to change to focus on getting the flare-up under control, getting the storm to move out as quickly as possible to get back to a nice day at the beach. And so the focus then becomes on pain control.

Everything we can do to provide analgesia to these patients through a multimodal strategy. And so what we want is to maintain these nice days at the beach as much as we can and avoid our flare-ups. But we have to understand that as part of the disease condition, these flare-ups are going to occur.

So we need to know to recognise those, and we need to know what to do when we find patients in a flare-up. So what are owners gonna complain if, if they come to see you, and they are noticing issues with their pet? Well, they might complain of a reluctance to exercise or stiffness.

Maybe they warm out of it, maybe they don't. Maybe there's a consistent lameness or an intermittent lameness. Maybe they don't want to jump up on things.

Maybe they're starting to see changes such as they take the dog on the walk and the dog's starting to slow down or lag behind them, or the dog's reluctant to go up the stairs or jump on the furniture. Cats are a little different because remember they're not small dogs. They're gonna have very few signs, but they will show things like a reduction in activity or a reluctance to jump or an unkempt appearance or maybe even aggression.

The problem is, if you look in a feline textbook at pretty much any disease in the cat, it's gonna list these four clinical signs. So it's not a slam dunk. To having osteoarthritis in the cat.

So, for example, in this video, you can see how this cat really hesitates initially to jump up on that chair. And so this cat should just be able to jump right up on that chair, but by hesitating like he is, that tells me something's hurting on this cat. Something's bothering him and we need to figure out what this is.

And so, let's ask ourselves a few questions. So first and foremost, if, if we look at strictly just the history and, and the clinical signs that the owner is describing at home or that you may see in the examination room, can you diagnose a patient with osteoarthritis at that point? I think the vast majority of us would say, no, we, we need to put a hands on the dog.

We need to do an orthopaedic examination. What might we find? Well, if there's a loss of usage of a limb, we might see muscle atrophy, as you can see in this patient here that has loss of muscle mass of the left hind limb compared to the right hind limb.

We might see joint swelling or, or extracapsular fibrosis. The best example here would be medial buttress from a cruciate ligament tear. Joint effusion.

There can certainly be a reduction in range of motion. If it's been going on for a long period of time, we can see crepitus and pain. And the reason I have muscle atrophy and reduced range of motion bolded and underlined is I'm a big, big fan of getting as much objective information as you can.

And so, just because we look at a patient and say, yup, there's muscle atrophy there, the question is, well, how much? And so, measuring muscle circumference with a tape measure is a great objective means to say, OK, I have a 2 centimetre muscle mass difference. If I institute a management strategy and I recheck this patient, then I know, I, how are they're doing?

Are they getting better? Are they staying the same? Are they, are they getting worse?

Because when people say, yeah, if I treat patients with X and they get better, my next question is, well, how do you know? And using objective information is the best way to do that. And so for range of motion, for example, we can measure joint angles and joint motion through the use of goniometry.

And so I can measure hip extension and if normal is around 160 degrees, well, a dog could have 155 degrees of hip extension, and that's considered abnormal, but it's probably not clinically relevant. But if that dog's got greater than 10 degrees of loss of range of motion, that's probably more clinically relevant. Cats are a little hard to examine because we can't just hold them down and, and treat them like we do in Dog, I like to watch them walk and move around the exam room.

But most cats are willing to jump off an exam table pretty readily to get into their carrier. So I like to see how readily they want to jump. So, for example, if they hesitate or they don't want to jump, that can certainly be a sign of discomfort in this cat, that they don't want to jump down and put that excessive force onto, the limbs, that may be bothering them.

And so the next question then is, can we diagnose a patient with osteoarthritis based on history, clinical signs, and orthopaedic examination findings. And while I think realistically, the answer has to be no, in the day to day practise of, veterinarians, this is usually where a lot of patients get stuck with a diagnosis of osteoarthritis and they don't always go to the next steps. Which the next step is we really need to get some form of imaging, which commonly is radiographs, but we have to understand what the limitations of those X-rays are, meaning they only provide bony information.

So we're looking at things like osteophytes or sclerosis. Osteophytes are useful to diagnose osteoarthritis, but they're not pathogomonic and the value of trying to take a radiograph, say today and follow up in 6 months or a year to look at the progression of osteophytes, to say that there's progression of OA is a bit controversial. And remember, it doesn't correlate with clinical signs.

So while we can say that the patient has osteoarthritis, what if they're in a period of continence versus what if they're in a flare-up? Our management strategies are gonna be very different. And then remember our radiographs are non-weightbearing, so we can't make conclusions based on joint space narrowing, and how much changes there may be.

So let's look at an example here. This is a feline pelvis, and they themselves can have evidence of hip dysplasia. And so on the left side of the white dotted arrow, we might see osteophytes of the cranial cranial acetabular rim or on the right side where the black dotted arrow is, we might see what's called a caudolateral curvilinear osteophyte.

And this is a little subtle line that can develop and we can see this in in dogs with hip dysplasia very young. As young as 67 months of age. There's also what's called a circumferential femoral head osteophyte, which these are little patchy areas of changes on the femoral head, where in the neck, where the joint capsule attaches.

And, and the combination of those two changes we can recognise very, very early in a, in a puppy to determine does this dog already have radiographic evidence of, of osteoarthritis. The elbow is, is one that really is a bugger for, for all of us to deal with and, and what we might see the orange arrow, osteophytes off the radial head, in about 30% of dogs with, with elbow OA. About 70% of dogs with the green arrow are gonna have some osteophytes off the inkial process.

But even before we start to see osteophytes, what we'll see is subchondral sclerosis of the ulnar notch or this blue arrow, and that tells us that that bone is being loaded abnormally and there's something abnormal going on inside the joint. But the problem is, is when we talk about radiographs not correlating to clinical signs, this is a radiograph of an elbow of a patient that has very mild osteoarthritis. There's some changes off of the radial head.

There's not really any changes off the process. There is moderate subtrochlear sclerosis. And so I don't want to look at this radiograph and think, OK, this dog's only got some mild arthritic changes.

Let's go ahead and start managing them. Because if I put a camera, and this is this dog's arthroscopic video, we can see that there's a fissured coronoid process at the probe here that's moving. But more importantly, if we look at the base of that, there's no cartilage on the base of the coronoid process.

And then if we move and look up at the humeral condyle on the medial aspect where it articulates, there's also no articular cartilage. And so this dog has end-stage medial compartment disease but only has mild radiographic changes. And so remember that radiographs aren't always gonna tell the full picture of what's truly going on inside that, that joint.

In the stifle, we might see with the orange arrow joint effusion where we get compression of the, of the fat pad cranially. We'll see some changes of osteophytes off the distal pole of the patella, or in the light blue area, osteophytes at the proximal border of the trochlear groove or even at the dark blue arrow osteophytes off the caudal tibial margin. And this is pretty common for the dog with a cranial cruciate ligament rupture.

And so from a diagnostic standpoint, what we really want to start thinking about doing is moving from a retroactive approach to OA management to a proactive approach. Meaning, if we're waiting and then we see radiographic changes of OA, we're way behind the eight ball. We need to figure out, can we pick out these patients before that period of time?

And therefore allow us to institute things earlier in the stage of disease rather than trying to play catch up. So this is where I love to introduce the concept of what's called the coast approach or the canine osteoarthritis staging tool. And I think this is a very valuable, thing from an objective standpoint that you can add in to these patients.

Because this is a staging tool for clinical management of osteoarthritis. And not only that, but what I really love is it allows recognition of at-risk patients before the onset of clinical signs. And then it allows you to follow up with these scores to guide management efforts.

And so what happens is this involves the owner filling out a, a, clinical metrology index, maybe the canine brief pain inventory index, the CBPI or the Liverpool OA score or some other type of, of score, the orthopaedic canine orthopaedic index, for example. You as the veterinarian, are going to grade the dog based on the discomfort and the posture and the motion. But also the particular joint, is there pain upon manipulation.

And what is our examination findings? This is where we can put in our goniometric measurements. We can put in our thigh circumference or our forelimb circumference measurements.

We can also grade the radiographs, and then we're gonna take that and figure out, is this dog in a pre-clinical stage where they are a grade of 0 and they have no OA risk factors. Is this a dog that's clinically normal, but they have OA risk factors, or is this a dog that already has mild, moderate, or severe issues? And what I really like about this is this recognition of the grade one, because these are the dogs that we may otherwise completely ignore until they present to us at skeletal maturity or sometime after when they're starting to have radiographic issues and clinical signs associated with OA and we've missed a lot of time that we could have intervened.

And so what this would look like from grading the dog and the joints and filling out the clinical metrology index will get a grade. So for example, this would be a dog with moderate OA, then you can institute a management strategy and in 4 or 6 or 8 or 12 weeks follow up. Repeat this to see, is it Getting worse?

Is it staying the same or is it getting better to help us figure out, are we getting these patients out of a flare-up? Is this patient in a flare-up? Or how's our management, strategies working out?

Because when we want to manage something, we have to set goals for what we want to achieve. Otherwise, we're really just sort of blindly going after things. So when we ask ourselves what we want to achieve, maybe we want to improve quality of life.

I think all of us would agree that's a great goal to strive for. Certainly to improve pain and, and maybe is it possible to decrease flare-ups when we get these patients out of them, improve their daily activity, go back to improving the human-animal bond. So owners used to love to go on a walk with the dog, can we get back to doing that so they can do those things they enjoy together?

Decreasing body weight, And I, and I think once we define our goals, then we have to lay out the pathway for how we're going to accomplish this. And, and with osteoarthritis, it really has to be a patient-centered and specific approach, not a cookbook approach. We can't just follow a guideline because every patient on the OA spectrum is gonna be at a different point in the course of disease.

Some patients may be in periods of remission with mild changes. Some patients may be, in a flare-up and they've been in a flare-up for many years. We've got to try to decipher all of this information.

To say what's best for this patient. And so it really needs to be a multi-modal approach from things like our anti-inflammatories and our analgesics and considering the joint supplements play a role versus physiotherapy on both an at home versus a formal basis and daily exercise and what that means. Maybe we actually inject something into the joint to provide relief or maybe there's something we're missing.

For example, a lot of my research years ago was looking at how oxidative stress affects canine chondrocytes and, and this aspect of free radical release and scavenging. And does that play a role in osteoarthritis? And if so, how do we manage that?

Or maybe using things like omega 3 fatty acids. Or the big thing to ask ourselves is how many of us have seen an overweight or obese dog. At least in the United States, there's approximately going to be about 60% of patients, I'm sorry if you hear the dogs barking in the background, somebody just rang the doorbell.

But ultimately, you know, when we Look at weight reduction, basically, what we're thinking about, is trying to get weight off of these dogs because as I was saying in the United States, about 60% of dogs are classified as being overweight or obese. And so that's a huge problem we need to try to address. And so the way I approach these patients is I really try to make it easy and break it into two separate categories.

I first ask myself, do I have a patient that, you know, has a primary problem? Maybe this dog has a cruciate ligament tear, or, this is a patient that, has what I call incidental OA. Remember the dog that comes in with acute gastroenteritis, and we find that they have Osteoarthritis.

But they don't have any clinical signs at the moment, or those with the pre-clinical OA from our coast form. So for example, the 6 month old puppy with developmental elbow disease. So what are we gonna do with these patients versus the patients that had a primary problem and now suffer from osteoarthritis?

So these are the ones that have the typical OA consult. The ones, that come in for maybe they're slowing down a little bit or they don't want to, to get up as, as, as easily or, or maybe they're having trouble going up the stairs or, or they're starting to self-limit. So, so something's changed.

And so when I try to break these down, my approach to these are gonna be slightly different. So, for example, the ones that have a primary problem. And have or will develop a way or they have the incidental or the pre-clinical way.

I think a co evaluation is very, very important. And so here's where we want to be proactive, not retroactive. But it's also very important to give owners clear expectations of the future and warn them that even if we get things under control now, flare-ups are going to occur.

So, for example, if I have the dog with a ruptured cranial cruciate ligament, it really doesn't matter what procedure I do to stabilise the stifle, there's going to be osteoarthritis in the future. And so I need to go ahead and talk to the owners about this and warn them of flare-ups. And so we're gonna work on establishing our baseline.

And this is where we might think about the incorporation of joint supplements and our omega 3s and our disease modifying OA agents. We want to promote daily activity, in particular, And those patients with the incidental OA or the pre-clinical OA, meaning what we want to do is, if these patients are not in a post-operative period promoting daily activity and managing weight through the combination of diet and daily exercise. And so with this group, those that have the primary problem and could develop OA or the incidental OA or the pre-clinical OA.

This is probably where we can have the most profound effect on the course of disease. Again, trying to develop that proactive approach versus the retroactive approach. So these are these patients.

These are the patients where life is good, we've got a day on the beach. And so when we start thinking about some of these aspects of establishing the baseline, we can talk about joint supplements, for example. But it is one of these things that we need to be careful of because it's a deep, dark world, just to tell the owner, hey, go start your dog on a joint supplement.

So if we're gonna go and recommend joint supplements, we want to make sure that what we're using is a product that meets label claims. So in the United States, they don't have to have, FDA approval. And I understand in Europe, there's also the ability for companies not to meet label claim.

And unfortunately, a lot of companies just don't meet label claim. And so we want to use a product where we know that when it's tested, It meets label claim each time. And then also products can differ.

And, and so, for example, chondroitin sulphate alone has a very poor bioavailability. And so what that means then is, with certain brands in the combined glucosamine chondroitin sulphate, there can be a synergistic effect. That's not true for every, company out there.

And then when we look at, using it in patients before the development of, of osteoarthritis, there's actually a study in the American Journal of Veterinary Research in 1999 where they took dogs, and this was a laboratory-induced model of carpal synovitis, and they started a group on dogs on cosaquin before the onset of carpal synovitis, a group That was started on after and then a group that was the placebo and based on their outcome measures, the group that had the best outcome was the group that was started on the supplement prior to the onset of synovitis. And so, again, I think we want to make sure we're using a product that meets label claims, that's tested, and it has some quality assurance behind what the ingredients in that product is. We want it to be very high quality.

And so, a few other things. For example, when we look at Daoquin and, and why I tend to like Basoquin. So the glucosamine and chondroitin sulphate, within Dasoquin is, is great.

We do get that synergistic effect, to increase bioavailability for chondroitin sulphate. But the other thing that's nice about Dain is the avocado soybean on Spottifiable in there. Because as we can see in this graph.

So if we take canine chondrocytes, and, and we have the control group, on the far left, and you see that the, the prostaglandin E2 levels are very low. That's an inflammatory marker. If we take those cells and we inflame them by inducing inflammation with what's called interleukin 1 beta, we can see a huge increase in PGE2 concentrations.

But by using the combination of, of avocado, soybean, and Spottifiable. So ASU along with glucosamine chondroit and sulphate, we can see a significant reduction in inflammatory mediators in the form of PG2. That's gonna be that pink bar.

But the far right, sort of that really bright, reddish pinkish, One is with the addition of Boswellia. And that's also in Daiquin. And what's nice about that is with the addition of, of the Boswellia with the avocado soybean that's spottifiable, and the glucosamine and the chondroitin sulphate, we've seen an even 30% greater reduction in inflammatory mediators.

So again, it's all about reducing inflammatory. Changes. Now, I do think it's wise to, to note that these are done in laboratory studies.

However, there have been studies done looking at bioavailability and uptake showing that, some degree of the joint supplement is going to be making it to the joint. But that can't be said for every product because not every product goes to those lengths of testing. Now, omega 3 fatty acids, I think we do have a bit more clinical evidence associated with these as far as what's going on.

Such that we're going to be all about controlling and decreasing inflammation. And so, interestingly enough, canine chondrocytes have the ability to selectively store what's called omega 3 fatty acids in the cell membrane phospholipids. So it'll actually create or compete with the acheddonic acid.

And if we do have release of inflammatory mediators, omega 3 fatty acids can help inhibit the release of things like cyclooxygenase and lipooxygenase. But the big question that tends to surround the usage of omega 3 fatty acids is really what's on the dosage? And, and what we see, this is a study by a nutritionalist in the Journal of American Veterinary Medical Association looking at what's the approximate dosage of omega 3 fatty acids.

And, and we find that it's actually high. Higher for OA than for some of our other conditions. And so for the daily dose of EPA and DHA, we really need to be thinking about 150 to 175 migs per gig daily of, of omega 3 fatty acids.

And so that can be obtained through, liquid that's put on. To the food and then depending on the diet, it can also be acquired within the diet, assuming that the diet has a high level of omega 3 fatty acid, and we can ensure that trying to get that high level of omega 3 fatty acid, we're not adding additional kilocalories by having to feed more kibble. The other thing too is, is our polysulfated glycos aminoglycans.

And so, at least in the United States, we have approved what's called Aequine. And this is a disease modifying OA drug, that's labelled to be given as intramuscular injection. And the dosage of this is designed to be around 2 migs per kg of body weight, twice weekly for 4 weeks, so a maximum of 8 injections.

That's what the studies were based off of an 8 week old puppies with hip laxity. Antecally, somewhere along the way, we decided that monthly injections would be OK. And so we now see that happening more frequently where patients will be loaded on it and then they get in, on a, on a monthly basis as we proceed.

That it, that it helps, but there's really minimal to no evidence to suggest that doing it monthly is going to help. Now, ultimately, I think for it to be as effective as it can be, it needs to be started as early in the disease process as, as possible. Now, the mechanism of action is really not known.

We know that it's gonna inhibit various proteases and, and stimulate the production of, of collagen and hyaluronic acid. And we can give it off-label, at least in the United States, as long as owners understand that it's designed to be given intramuscular. There is evidence to suggest that the pharmacokinetics, at least of Aequine, are similar if it's given, in a sub-q manner versus an IM manner.

We can also use it in the feline, but again, it's, it's off label. So we just need to make sure owners are aware of this. Now, weight control is going to be probably the absolute biggest component to this in daily exercise because we know that obese dogs require more OA, they require more analgesia, and they have shorter lives.

And so our goal needs to be to reduce the load and the stress on the joints. And we're gonna do this. Through the combination of reduced caloric intake, but also through regular exercise.

Now, if we think about people, for example, we can go on a diet and lose weight, but it's not sustainable for life. What we really need to do is combined appropriate diet with exercise. But what owners have to understand is that running around the backyard is not exercise.

That's daily playtime, which dogs need, assuming that they have minimal arthritic changes and that running around the backyard is not going to induce, a flare-up. But daily walking is the absolute best form of exercise. And, and the goal being, if we can, to build up to 20 minutes on level flat ground twice daily, But the other thing we need to think about too is lifestyle changes.

And that doesn't get talked about a lot because if we have patients that have arthritic changes, we don't want to do activities with them that are going to put the joints in a constant repetitive concussive force. We want to change up our lifestyle habits, maybe think about our flooring where we have better, Grip flooring, so whether that's rugs or yoga mats, minimising stairs, minimising jumping, and try to find activities that the owner and the dog do together that promote daily activity but not, excessive forces on the joints. And if we want to try to get weight off of a dog, we want to shoot for about 10% of body weight at 1 to 2%.

Weekly. And, and this is what I call a Davidism, meaning there's not canine evidence to suggest that getting 10% of body weight off a dog with OA is going to have a profound effect. However, in people with knee osteoarthritis, if you lose 10% of body weight, it can, have a profound effect on your stiffness and your discomfort.

So, the other thing now is moving to those patients that had the primary problem and now they suffer from OA. So this is group 2. So in, in other words, the dog that had a cruciate ligament tear, we repaired it years later, now we have arthritic changes, or the dog that comes in for the slowing down or the stiffness.

Well, We can continue our baseline if indeed we had already established that baseline. The trade-off being if these patients are painful and in a flare-up, we have to stop the daily exercise, and try to get the flare-up under control by focusing on analgesia. This is where our non-steroidal anti-inflammatories are going to play a massive, massive role.

If we think we need some form of opioid, I tend to use codeine. I don't use tramadol. However, in general, I don't think opioids really have much of a, of a play in, in long-term management.

Amantadine is a really nice drug, when it's combined with an anti-inflammatory or some other analgesic. And actually, it's outside of an NSAID, the only, drug that shows relief of joint pain, from an OA management standpoint, that can be given at 3 to 5 weeks per cake every 12 to 24 hours. Gabapentin is another drug that's gaining popularity and usage, at least in the United States.

We don't have any clinical, evidence to say that gabapentin has a profound effect on joint pain. But from a central sensitization of wind-up standpoint, I do think it can play a role, when, needed. And so, these are the patients where life isn't good.

These are the patients where they're painful, they're hurting, they're not able to have a good quality of life, and we've got to do something to help get them out of this. This flare-up. One of the things that I would encourage you to always remember is that you never want to make irreversible decisions such as surgery or euthanasia in a patient in a flare-up.

The goal needs to be, can we get the flare-up under control first and either establish a baseline or get back to our baseline. If that's not achievable, then we start thinking about irreversible decisions. And so what OA management is not is what we've done for many years.

Here's your anti-inflammatory and your tramadol and that's really all we can do. There's so much more that we can do. We can absolutely do better.

First off, our goal is to use NSAIDs at the lowest dose possible as infrequently as possible, knowing that at some point in the future, they're probably gonna need it on a more of a daily basis. Opioids are not designed for chronic use. And then there was a beautiful study published in the Journal of American Veterinary Medical Association in 2018 showing that in the canine, tramadol has zero benefit for joint pain, compared to a placebo.

In the feline, however, tramadol can have a benefit. The problem is trying to get tramadol into a cat because of its bitter nature. But also don't lose in the follow-up.

Don't just represcribe and re-prescribe and not get them in. You want to get the initial information and then institute a management strategy, get them in 2 to 4 weeks later, recheck them, see how they're doing. And if things are progressing, get them in 6 weeks later and see how they're doing and once they're out of the flare-up and once they're comfortable, then get them in every 4 to 6 months for man for, for evaluations because this is long-term, lifelong.

Chronic pain management. Now, owner education is going to be, I think, probably the biggest component. They need to know that this disease process is progressive.

So we might have to reestablish our baselines as the disease is progressing. If your dog can go on a 40-minute walk now, it might be that later down the road, we have to reexamine our expectations for daily exercise based on the condition of the joint. And no matter what we do, flare-ups are going to occur.

So we need to let them know if you've established the baseline and then the dog starts to deviate from the baseline, that can indicate a flare-up. And then they need to understand that management is step-wise. So, what you may start now, may not work in the future.

And so it's gonna be ever evolving. And if you really have this conversation with owners and really get them to understand that this is a multimodal progressive management, then it starts to become a little easier when things become less effective for them to understand. But what are some other things we can do for these patients as far as thinking outside the box?

Well, I think physiotherapy is a great addition. Think of it as another tool in the tool pelt to help manage pain and, and restore and maintain function, restore and maintain range of motion. And slow down and minimise the progression of a way.

Because here's probably one of the most important takeaways from this entire talk is that maintenance of range of motion is critical. It is directly correlated to limb function. So if a patient has a loss of range of motion that's gonna have a direct effect on function.

And if we have patients that we're not doing things to actively promote range of motion, they're gonna lose it, which means they are going to deteriorate quicker. And so from a rehabilitation standpoint, with patients during a flare-up, we can do things to maintain range of motion, but not induce discomfort while doing that. And I think that is a massive, massive take-home point that we need to recognise is maintenance of range of motion is paramount and it's so much harder to regain range of motion once it's lost.

Other things we can think about, what about intra-articular injections or other injections of things? And the nice thing about intra-articular injections is that every one of you can do this in daily practise with minimal equipment and training. What it takes is a little bit of learning, and there are a number of products that we can inject.

So for example, hyaluronic acid, I used to think, OK, it's just gonna help re-lubricate the joint, but what we find it also does is restore physiochemical properties to the joint. It's widely used in horses and humans for OA. And when we look at the molecular weight, what we see is that dogs have a relatively low molecular weight compared to horses and humans.

And what this means is that we can use a dog product in the dog. We can use a human, or I'm sorry, a horse product in the dog, but what we cannot use is a human product in the dog because that would cause a big flare-up. But in patients with osteoarthritis, Because the synovium is affected and the synovial fluid is being produced from the synovium, the molecular weight is, is decreased.

And more than just re-lubricating the joint, what it's going to help do is stimulate chondrocytes, start producing extracellular matrix, stimulate the synoviocytes to start producing healthier syno hyaluron. It's also gonna act as a bit of an anti-inflammatory, and then block certain proteases. And so, Hyaluronic acid is typically given at a dosage of about 15 milligrammes to 30 milligrammes in the joint.

We don't want to give it necessarily IV because we haven't seen a, a profound effect on giving it IV. I would not give it sub-Q because hyaluronic acid is in the cell membrane of most any tissue and it's likely gonna stay very focal there, but it's not gonna get to the joints. Another thing to think about would be steroids.

I know a lot of people are like, oh my goodness, steroids are taboo. But not always, cause it can decrease pain and inflammation by reducing synovial blood flow, altering the inflammatory response, and altering local collagen synthesis. And so I have no problem at all reaching for an intra-articular steroid injection.

But for me personally, I don't want to use methylprednisone or Depo-Medrol unless I've got a very geriatric or end-stage arthritic joint where I want a little bit longer duration. If I'm gonna use Depo-Medrol, for example, I might use 20 milligrammes of the joint versus trying Simalone, which is gonna be my go to. I'm gonna try to use 5 to 6 milligrammes per joint, and try not to go over about 18 milligrammes total if I'm injecting, multiple joints.

From the studies, we know, I, I, I probably wouldn't say it's safer. I would just say it's probably less chondro-destructive than our other anti, or our other steroids. In at least in the United States, we also have this concept of synovial rhythus.

This is the injection of a, of a radionucleotide, that directly targets synovitis. And, and what it does is it helps diminish pain and inflammation. By causing phagocytosis of the pro-inflammatory macrophages and synoviocytes.

This was just launched this last year in the United States. I'm not sure of the company's desires to come abroad or not, but that's another concept to consider from an intra-articular management standpoint. At least in the, in, in the UK you guys have anti nerve growth factor that was just released.

We do not have this in the United States and I'm a bit jealous. I, I hope that we get it soon. Because what this recognises is that with a nerve growth factor being released, it not only causes pain at the joint, and, and sites an inflammatory response, but it's also responsible for this concept of driving central sensitization.

And so, an injection of anti nerve growth factor, is, is hopefully a really nice thing to, to add into our toolbox. And I would really, really love to hear, from those of you that have used it, what your experiences have been and, and how well you think it's working because I don't have the personal experience of getting to use it yet. But when we look at intra-articular management, the dog, it's, it's actually quite simple.

We just want to shave up an area. We don't have to be as sterile as we are in the horse. We're gonna aseptically prep an area.

This is just in my treatment area under a light sedation. And then once we learn our landmarks, which can be based off of textbooks, and, and then you can practise, once we pop into the joint, this is a hip, for example. What we're gonna do, is once we're in the joint, we're gonna attach a syringe and we're gonna remove the joint fluid, cause that's gonna be full of inflammatory mediators.

And that's also gonna help us know that we're actually in the joint where, we should be. And so, what we'll do is, is we'll remove the joint fluid. Once that's removed, then we'll inject our product.

And so, this is Going to be tryingimolone going into the joints. And once that is put in, and it should go in very easy. There shouldn't be any resistance when we're injecting it.

Once that syringe is removed, then I'm gonna take my syringe of hyaluronic acid, and I'm going to inject that. So that way I have, a combination of a steroid and hyaluronic. In this joint.

Once the injection is done, once I start to feel a little bit of resistance, I know that I've got the maximum volume I can get into that joint. And so then I'm gonna remove my, needle, and I'm gonna run my joint through range of motion, and then I'm just gonna reverse the sedation and the patient's gonna go home that day. So it's very, very simple and easy to institute and gives you another bit of arsenal in your tool belt.

And so, how long do we expect for these things to last? Well, hyaluronic acid will have about a 4 to 6 months of relief. That's when it's given as a series of 3.

You give it once a week for 3 weeks. About 75 to 80% of these respond really well. For synovialesis, we actually, from the studies see about 9 to 12 months of relief.

And that's what's really nice about this. B anti. Nerve growth factor, the way I understand it, it's about 4 to 6 weeks.

Steroids are a bit unpredictable, and what we didn't really hit a lot on is this concept of regenerative medicine because that's a whole day's worth of lectures. The concept of platelet rich plasma and stem cells, we might see about 3 to 6 months. And if, if somebody has more of an interest in my thoughts on this, and when we get to the Q&A in just a moment, please, bring that up.

So our take-home message for intra-articular management, if a patient's following the baseline, we're going to stay the course. But if they deviate from the baseline, this may indicate a flare-up. So we want to take a step back and figure out how to get that under control.

And so for me, I'll commonly use an intra-articular injection with pharmaceuticals and a period of rest for about 1 week to 2, and then a period of formal physiotherapy for about 4 to 6 weeks to try to get them back to baseline until the next flare-up occurs. And the best way to avoid flare-ups is to avoid what's called the weekend warrior syndrome, where the dog's lazy during the week and then the owners try to make up for it, on the weekends because the tissues are not conditioned for this sort of rest and then prolonged activity. So it's better to be active every day.

We want to focus on more frequent but less duration of, of activities. And then the last aspect that even though I'm a surgeon and love surgery, The very last aspect would be a surgical consideration from either fusing the joint or a salvage procedure such as a femoral head and neck ostectomy to potentially a joint replacement. But simply flushing and debring the joint is, is not recommended for the lack of improvement due to the morbidity associated with that.

And so, our, our management summary here is if we have those patients that may develop osteoarthritis, we wanna establish that baseline is Early as possible, through our joint supplements, our omega 3 fatty acids, daily activity and weight control, taking a patient specific and owner education is, is key. This is where a coast form is going to be very much helpful in the management strategy. If we have those patients that have OA and they're not in a flare-up, so the incidental away, then we want to establish the baseline.

But if we have those patients that have a way and they are in a flare-up, well, we can establish a baseline, but we have to be cautious about the activity portion of it, and we need to do things to get pain under control through anti-inflammatories, analgesics, physiotherapy, intra-articular injections, . And then that flare-up gets under control, excellent. We initiate our baseline.

If that flare-up cannot get under control or it's becoming more frequent, we're gonna circle back around and say, OK, maybe I tried an anti-inflammatory. Maybe at this time, I'm gonna move to an intra-articular injection and rehabilitation therapy. But if we're still not able to get that under control or we're seeing recurrent bouts that's affecting the patient's quality of life, that's where we would then bring in, a surgical thought process.

And so with that being said, I, I certainly apologise for the bit of technical errors right before. I, I have no idea what was going on. But, what I'll do is I'll stop sharing my screen in just a moment and then I've got some time to answer some questions.

If you're an individual that likes social media, my, Instagram and Facebook handles are, are listed here. My email address is also listed here as well. If you have any particular questions, please, please feel free to, to email me.

It may take me a little while, but I promise I will get back to you, to answer your, your questions. And so again, I very much appreciate you taking your time out of your evening for, allowing me to present to you guys. And I will just say I, I wish, there was the ability for us all to meet in person, travelling over to Europe is one of my most favourite things to do, and, and I miss it dearly and I'm so ready for restrictions to be lifted so that I can get back over there and hopefully be able to meet and socialise with, with all of you.

So I'm going to stop sharing my screen now, and then I think we can tackle some, some questions if, if there's any that have come across. That was great. Thank you so much, David, and I, and I think You know, go back 30 years and it was a bit of predanleukotrophin and phenylbutasone, and it's so good to see this multimodal approach that obviously, you know, as dermatologists, we do the same thing and, and also to see this sort of similarity with hyaluronate, sodium hyaluronate being a bit of a wonder drug as well.

I use it for my, for my eyes and as you say, it also helps. Getting the cornea sys going and everything, so, yeah, there's some really interesting stuff, just using one drug, doesn't give you the control and, and you are a marvellous surgeon who doesn't immediately reach for reach for surgery, so. I think the rehab and stuff is, is really good, we've done some webinars on that and I think it's an area that, Tennessee is really leading on and it, it's great to see that, You know, in the UK certainly we're starting to, to learn and and catch you guys up, so thank you so much for a fabulous webinar.

Absolutely. My, my pleasure. We've had some some questions and also just a few people telling us where they are listening in from.

So we've got er Holland and er we had somebody in San Diego, which is really exciting as well, and Qatar, South Africa, Mzumbe in South Africa, and Scotland and Romania, so really nice to see people putting in where they're, where they're from as well. So questions, yeah, we've got a few, these are, some of them are slightly longer because of course trying to give a bit of history as well. So I, I'll start with James's question.

Thank you, David. What would you consider as the main reason for the dogs to develop OA? Do you think it's more of a genetic issue, or is it due to the lifestyle?

For example, a puppy it's too heavy for its choice but still receives a lot of physical exercise. I understand both reasons are the possible culprits. What I want to clear up is if my puppy, German Shepherd Dog, 14 weeks, has a normal walk, he trots mostly, not jumping, not a lot of running, about 35 minutes in the early morning, a couple of quick.

We walk during the day and then another 30, 40 minutes, the same way as the morning. Would it be an issue? He looks fine, and I try to use a common sense approach instead of following a rule of 5 minutes per month.

Gee OK, don't know where this rule came from. His parents are in good health in terms of joints. He's not allowed to jump and go downstairs.

Do you think he's at risk with this regime? Wow, a lot, a lot there. So, so, to, to break some of it down, I, I think a vast percentage of, of our dogs develop arthritic changes, secondary from some form of developmental, diseases, whether it's a developmental elbow disease or, or hip dysplasia, .

I, I think dogs that are oversupplemented as puppies are going to be at risk for orthopaedic diseases. Dogs that, get overweight are going to be a higher candidate for, arthritic changes. Dogs that tear their cruciate ligament have intra-articular fractures or have fractures that maybe as a puppy that was trying to manage by external coactation and there is a malunion.

So now the joints being loaded abnormally. That's gonna be a reasoning. There, there's a lot of, discussion around this aspect of puppies and how much do we exercise them, what do we let them do, what do we not let them do.

And there's minimal to no evidence on, on really any of these recommendations. So I'll, I'll give you mine and and some people may completely agree and disagree with me, but you're not gonna have the dog develop osteoarthritis by letting them go downstairs or wrapping them in a bubble and not letting them do anything. I'm not a fan of forced exercise on puppies.

Usually, what that means is when they're a puppy, training them to get used to walking on a leash appropriately in basic commands. So if they're gonna go for a walk, we're gonna minimise the time, but we're gonna let the puppy choose the pace as we're instructing them that a pull on the leash. I'm not gonna force a brisk walk.

I'm not gonna force a fast walk. And then I will typically allow them to socialise and play as, as they see fit. But with play being more constructive, not, not play that is going to then lead to a lifetime of, of chasing the ball down a slick hallway and sliding into the wall or a play where I'm gonna sit on the back porch and throw a ball and they're gonna jump off the deck and then run after it.

And, and so I do want to minimise concussive forces on, on the joints, but also start to set the play expectations for things that aren't going to put repetitive concussive forces on the joints because Time and time again, we'll have adult dogs that come in that have arthritic changes and we talk about stopping certain activities and, and the owners think, oh my gosh, this is what they live to do. Well, maybe if when they were a puppy, we had established other tactics of play, they wouldn't live to do some of these things that cause a lot of repetitive concussive forces on the, on the joint. So, You know, I think based on what was asked as far as with this particular puppy, I, I think what you're doing seems reasonable.

And I would not put what you're doing as an increased risk factor for your dog developing arthritic changes. As assuming that there's not any genetic influences for the predisposition for something that's gonna cause arthritic changes. Yeah.

But I'm just saying, hi, doc, what do you think about hydrolyzed collagen? Hydrolyzed collagen, you know, there, there's a little bit of evidence there. I, I assume this is going to be orally taken.

You know, again, it's, it's one of those things with, with a lot of aspects of things where I say, You know, it is, how much is it going to be helpful? Well, there's minimal to no clinical evidence, in clinically relevant studies. Is it gonna hurt?

No. Could it be helpful, possibly. And so if I, usually if an individual feels like it's, it's gonna be helpful, I'll say go for it.

As long as I know that it's not gonna cause damage or harm, then I'm typically OK with it. If they want to, but, but what I would not do is, is want an individual to put their time, money, and effort into something with minimal clinical evidence to neglect something with clinical evidence. That's where I might steer them towards an area.

But if it's, if it's in addition to the other appropriate management strategies, I would be OK with it. Great, that's, that's fine. We've, we've got another question, recas.

Can you suggest activities that cats with 0A or potential 0A should or should not do, especially re-jumping on and off high surfaces. Yeah, cats, cats are very, very difficult. And, and, and so what I would try to minimise is, certainly jumping on and off high, structures if, if that can be, done.

What I would do is, is over time, see if you can lower that. I think activities that require cats to not Accelerate, decelerate and turn quickly, but yeah, allow them to reach out bad at things, reach for things, those are all gonna be helpful to help maintain range of motion. You know, with cats being the way they are, it would be impractical of me to say to prevent all jumping, but maybe trying to create an environment to minimise jumping, so that we're not putting the cat in situations where we're encouraging them to jump on or jump off.

Can we train them to go upstairs to something versus jumping onto an object, or can we, get them used to jumping on several aspects to get to a high object rather than trying to jump all the way up or all the way down? Yeah. No, that's great.

Just so people know, there is a survey to fill in for tonight's session, which Dawn has kindly put into the chat. So if people go over to the chat and look at that, that would be fantastic. And everybody's suddenly telling us where they're, they're listening in from and, and David, you know, I know you were talking about physical meetings and, and the, The negative if you like, of webinars is you never hear the tumultuous applause at the end of your, your talk, so I just wanted to let you know that we've got And Kaloyan saying great lecture, thank you very much.

King is saying thank you. Er Ellie saying thank you, Rachel, thank you, Julia, thank you so much, greetings from Germany, Rachel's in Cheshire, Keith is in Grimsby. Which is in the UK, Wiltshire in England, Eileen, Jeremiah in Ireland, Alexandra in Greece, thank you, thank you.

Carlos in Switzerland, thank you and . Zack in Thessaloniki. So lots of people saying thank you and, and also, Bettina in Stafford in the UK as well and I suppose a final one, Alison in New Zealand, so she's up very early in the morning to listen to this, so well done.

But I I certainly appreciate it. Yeah, so really positive comments there. And then you're going to be jealous of Sean, David, because she says thanks for the great talk.

I've had a brilliant response to Librella monoclonal antibodies with my 12 year old lab with lameness and spondylosis pain resolved in the same day. Previously struggling on amantadine and Galiprat, and GIT disease was preventing the use of non-steroidals, also seen an amazing response in a nurse's dog with spinal issues and arthritis with severe hepatic disease, previously on Galipram, tramadol, and gabapentin. So that sounds really positive, but obviously a, a fairly new drug drug with with us as well.

You're, you're copying the . The dermatologists and, and coming up just second to us after we had that month. So yeah, it's really good, some of the stuff that Zoettas are putting out there.

Well, I'm, I'm thrilled to hear the, the positive response. That that's, that's excellent. Yeah, brilliant.

Let me see, we've got . And I, I saw, I saw a few things you want to, yeah, no, I saw one, things from Dubai. I hope to visit Dubai in November for a conference.

I've never been, . France, yeah, I mean, these are beautiful, beautiful places I think you all for attending. So, a couple of things.

I, I saw several people asking about, eye injections with platelet rich plasma, and so what I'll say is, is I do think platelet rich plasma can be effective. But when we look at the clinical evidence available in, in client owned dogs with naturally occurring disease, the, the problem is, is, is knowing what's in that product and, and is it going to be effective for a dog with mild disease versus moderate disease versus severe disease and how frequently we give it. For me, if I'm going to use a platelet product, I would probably think about a series of, of, of injections, at a minimum of 2 space probably about 2 weeks apart.

And then maybe up to 3. On the human side, talking with some sports medicine individuals, they usually won't go over 3 because if they're not getting a response by 3, that patient's probably a non-responder. As far as stem cells go, I think that's a very murky area where the clinical evidence, doesn't really exist to justify the cost at currently.

Especially when we look at the clinical evidence, only seeing about 3 to 6 months of, of relief, with usage of stem cells and also defining, actually what we're using as as a true stem cell can get a little challenging whether we're using a cultured versus an in-house processed, heterogeneous solution. So, I, I will use platelet products and platelet rich plasma. I don't, use stem cells or what's called bone marrow aspirate or stromal vascular fraction for, for OA management currently, that could change if, if we have clinical evidence that, that, supports the usage.

I noticed, somebody listening in from Texas, from Austin, so it's gonna be pretty hot there I would imagine at the moment, so, but . Also it's it's it's hot in Maryland, so I would . And, and, and I saw this one question on, on oversupplemented as puppies with what?

That's typically trying to get them to grow as quickly as possible to get as big as possible. Supplementing with things like vitamin D and calcium, those are no nos in developing puppies. There was a question about using this high of a dosage of omega 3 fatty acids, and any risk of pancreatic disease.

I, I'm glad this question came up. What I would say is, is in an otherwise healthy dog, I don't see, the induction of pancreatic issues with that high dosage. With that said, patients that have a history of pancreatitis, patients that are hyperlipidemic, I'm probably not gonna recommend that high of a dosage.

Patients that ultimately are breeds at risk for pancreatitis, I'm probably not gonna use that high of a dosage. And, and I do think that's important. The other thing to realise is the cat, we don't know what the appropriate dosage for the cat is, and we can't just simply extrapolate it to giving a cat a high dose of omega 3 fatty acid.

So I'd be a little cautious there. Also, There is sometimes concern about bleeding risk if if patients are on really high dose of omega 3 fatty acids with some people. I can't say that I've appreciated that, in the, in the canine, when operating on them.

So, so there is, is that, another question, David, which, I, I know John will be thrilled that you mentioned it earlier in his talk, so I texted him with the slides to let him know he's famous. Which of course we all know, yeah, exactly, you go, yeah, he, he's way more famous than I am. And he was talking, I think he's also talked in the past, about.

What are your thoughts on using pressure walkways for at risk dogs as a tool to help objectively detect mobility issues prior to visual clinical signs. Oh my gosh, I, I, I think it's, I think it's phenomenal. I, I think if, you know, with objective gait assessment, it started out looking at force plate analysis and kinematic analysis and things that were really only able to be done in either a university setting or a research setting.

But with the advent of pressure sensitive walkways and, and even a stance analyzer, which is a mat they stand on that will tell you how much pressure and statically is being put on all four legs. I think that's marvellous. If, if you, from a cost standpoint in a, in a space standpoint, it's now somewhat practical in first opinion practises to have that.

And if you do, so the practise as I work in, we, we have that and we utilise that on every patient at your initial consultation. But also at follow-ups to see how we're improving. And so if there's the ability to use a pressure sensitive walkway or even a stance analyzer, I think that's just another bit of objective information you can put in there to know if your patients are truly improving.

So that's, that's a great, great question. I, I don't know, David, if, if and Jemma may be shaking her head now whether Gemma wants to come on, put the, The camera on, obviously really pleased, Gemma, that, you know, protection has kindly sponsored this webinar. It's a massive, massive problem, and it's great to have David on just to take us through, you know, what's becoming a much more complex way of treating these than perhaps 20 or 30 years ago, but obviously getting, Much better results with this multimodal approach.

So, I don't know. Well, first of all, just again, thank you so much on behalf of protection for, for making this possible for so many people tonight and, and I'm sure many on recording over the next few weeks. The recording will be up tomorrow, so.

Obviously, if you've enjoyed it and want to show it to colleagues in practise, then it will be on the site as well. But over to you Gemma. No, I mean, absolutely.

Those that know us, and, and if you're in the UK or anyone that, that kind of deals with protection or even neutromax, obviously with, Daoquin in other countries as well. For us, we very much are focusing not just on the fact that, you know, we're, we're selling a joint supplement. It's very much when we go out and do educational programmes, it's always about multimodal because it doesn't work in isolation.

We know that from, from these cases. You can be extremely overweight and have all the non-steroidals and Well, but you're still not going to be able to get up on a slipy floor, or you will get into a car, or, you know, you, you're just not gonna get anywhere. I think, you know, as David said, they have the same problems in the United States as, as we do here, you know, and as a, as a company we really try and focus on.

Sort of the effort of as much evidence as you can get for these. And one thing we constantly get, and David, I don't know if you come across this, so people say, oh, studies about glucosamine and, you know, or it's, it's iffy and whether or not it's even absorbed or anything, and, and the one thing we found from all our research and, and obviously working with. Daoquin and and working with the guys at Neutromax is that when you're looking at a lot of these studies, as you said, molecular weights, bioavailability is very important.

The, the, a lot of these meta-analysis will literally look at studies where they say, oh, glucosamnochondroitin doesn't work. And I actually, when you look at it, it's looking at 50 studies and they've all used completely different sources, completely different molecular weights. You know, difference between getting a kitten and a shire horse through a, a cat flap in the gut, I, I say, you know, for bioavailability or into the joint.

But a lot of the stuff, even with sort of glucosamine, etc. Is a lot of these studies are done in healthy, healthy individuals. And when you look at glucosamine uptake, it, it often is sort of in a passive diffusion against a concentration gradient.

If you're healthy, then you, you, your glucosamine levels are good, you're not gonna have as good an uptake. So it, it's taken all of the evidence into account. But the big The thing and the most important thing is, is very much us.

If you come to us, you get anything from us or any nutraceutical company or any supplement company, ask to see that bioavailability data. Ask to see the evidence, that they've got for their specific molecule and their product, and they should always be happy to provide it. Ask for label claim evidence.

It's so, so important. So whilst we're regulated on ingredients, no one's really enforcing to make sure, you know, you've got the right. Amounts that you're saying and there have been studies, especially in America, I think, within the last few years that showed glucosamine and chondroitin products, and they took 10 products and basically only 1.5 even came close to me to label claims like you took the rest and, and from a company that's what what we say, always ask us, ask us for the evidence, ask any company for the evidence, whoever that may be, and we'll always be happy to provide you.

And, and I would just add, that, well, I was gonna add, oh yes, so also understanding what you're asking of the supplement to do, meaning, whether it's a glucosamine chondroitin sulphate supplement, whether it's a polysulfated glycose aminoglycine, whether it's omega 3 fatty acid. If you take a patient that comes in that is painful, that has severe arthritic changes, and they have severe clinical signs, and, and you say, here's your joint supplement and that's all you do, then of course, it's not gonna work because you're asking it to do not what it's, what it's designed to do. And, and so I think if you take that into expectations and incorporate it as the multi-modal management and not negate other aspects that are going to work synergistically, then I think you can have a, a better idea and that's what makes it hard in the research world because if you were going to conduct a study, you have to eliminate other biases, which means, OK, we need to stop these medications that are likely helping, and we're gonna use this aspect to, to look at, but we don't see an improvement.

Well, maybe because what we're striving to do, we're not gonna see because we're not providing pain relief in another avenue. So, again, I think that's where instituting these things as early in the course of the disease as possible is probably going to have the most profound effect. If, if we wait until an end-stage joint and then start something, we shouldn't expect to see much of, of a benefit.

And, and that's where early recognition and diagnosis comes into play. Could I ask you what what your thoughts are? Obviously it's very topical in activity monitors in this country at the moment, and, and a lot of countries.

And sort of from the research we've looked at, people go either way because they say, oh, a dog's activity has improved, so they've improved, whereas other studies are saying in activity has improved, it could be restlessness, agitation, and discomfort. So, sort of from the research perspective of an arthritis expert, where do you sit with that? Yeah.

I, I think there's going to be a lot of things we don't know about activity monitors yet. That we can gather some great information and, and if there's the ability to not just look at activity per se, but look at activity and what's, the heart rate, what's the respiratory rate, what are other parameters, then I think we can probably say, yes, this dog feels better. They are more active because of.

Versus this dog is restless or this dog is uncomfortable or unsettled. So, for example, monitoring sleep habits, you know, is the activity increased, but it's increased because the dog's getting up and changing positions because they're unsettled or uncomfortable versus the dog's activity increased during the wake hours, because the dog feels better. And, and so I, I think, just strictly looking at activity, it makes it a little hard to differentiate.

But putting other parameters into the ability to monitor would probably help pull some of that out as far as what's going on. And then maybe one final point. So when you talk about, everyone has the interest in intra-articular, and that's very new for us, I think that a lot more places are starting to do things like that have capabilities.

Do you ever find that you treat intra-articular one or two joints and then you notice an exacerbation in a joint you didn't maybe think was particularly clinical because they're feeling so much better in the other joints? Do you, do you ever find that at all? I, I can't say that I, I've seen an issue in another joint, .

Typically, with an intra-articular management, my hope is, is if, if a patient has 12 or 3 arthritic joints, then we're gonna be able to address those. And, and if I'm successful, that dog's gonna improve. The challenge becomes is when you have a lot of polyarthritic joints and you say, well, I can't necessarily inject all of these joints from a cumulative standpoint.

And so then you have to rely on your examination to say which of these joints that are going are causing the issue now to, to inject. And, and taking that approach, I can't say that I've had one come back that let's say we injected shoulders and elbows and then they've got hack away and they come back and now they're having a flare-up in, in the hock per se. That's not to say that couldn't happen.

I just haven't clinically appreciated that. Thank you. Just a few people asking about the recordings.

It's obviously on our website, the webinar vet.com. And if you've registered for this event, Dawn will be sending you an email so that you can just click on that.

You, you have to log into the site to watch the watch the webinar, but you will all, I presume, almost certainly have a username and a password, and if you log into the site. Then you'll be able to watch, from the link that you've been sent. Again, just reminding you about the survey link, so do fill that in.

Dawn has put that in a few times, and actually we've just launched our, we launch an annual survey every year, which just looks at, How are you finding the service, what things you want us to concentrate on? Do you want more talks on osteoarthritis or what are the areas you want us to cover? There is a nice prize.

You'll need to go on and have a look, but it's worth going on for. So it'd be really great if, if, you can give us your thoughts, because we want the service to be what you want it to be rather than what we think it should be. So, so do, do those two surveys as well, that would be a really big help.

. I don't think there's any more questions, I know . You've been really good to stay on, David. The, the nice thing about, webinars is people can slink off.

They don't have to stay till the end and be all polite, but, a lot of people have stayed on because, I think it's, it's really, some really fascinating questions that we've got here. I think we get about another 2 or 3 minutes and then I will get another, conference call. Yeah, well, let's just do this last one from Yost, who said, would daily management of low grade inflammation and osteoarthritis, even without clinical symptoms, not postpone onset of joint pain and or increase the non-flare-up episodes, next to the base management.

So I think. Yeah. This, this is actually a great question, to end on.

And, and I, and I think the answer to that is yes. The, the true answer is how do we achieve that? And, and what I mean by that.

Some could argue to say let's stay on an anti-inflammatory to keep the inflammatory changes at a minimal level. And when an anti-inflammatory is given an appropriate dose and monitored appropriately, it can be relatively safe. The other part can kind of say, well, Can we do other things to decrease the inflammatory changes and maybe we don't need the bulk of an anti-inflammatory right at this moment.

Maybe the inflammatory changes are small. That we can use something else to minimise that. And so, in particular, for example, the avocado soybeanspotifiable, the whole goal there is to decrease inflammatory mediators.

The Boswellia, the whole goal there, decrease inflammatory mediators. Omega 3 fatty acid is the whole goal there, decrease inflammatory mediators. So if there's a smouldering lower grade inflammatory response, the question then becomes, can we use those things to decrease it and then in a flare-up when the inflammatory changes are worse, we bring in the powerhouse of an anti-inflammatory.

Again, there's no hardcore concrete evidence to suggest one is right versus the other, but the concept of doing something to minimise the inflammatory response on a daily basis is absolutely the appropriate approach that we need to be taking. David, that's fantastic. Thank you so much for being so generous with your time, you know, after the, the lecture for the it's always an enjoyable part of every webinar, and Gemma, again, thank you so much for protect and for making.

This possible and I obviously thank you everyone for attending as well and we'll look forward to seeing you on a webinar very soon. So thanks again, David, and enjoy the rest of the day and I hope the dog gets out for a walk. We always like to.

So it was good to hear from him. Take care David. I certainly appreciate everyone's attention.

OK, bye bye bye bye now.