Transcription
Hello and welcome to today's webinar. My name is Felicity Thou, and I'm a physiotherapist and campaign manager within the Flip and Pain team.
Flip and Pain is a public health campaign, and we share the latest information about persistent pain and related conditions like arthritis with people affected by it and the health professionals who care for them. Today's event is the first in a short series of webinars collectively titled "Flipping Arthritis," which we suspect might change or flip the way that you understand and manage your arthritis.
This event is being funded by Haywood Middleton and Rochdale Integrated Care Partnership for people affected by arthritis across Greater Manchester. We're aware we have people joining us from further afield, and you're all very welcome. Today's event is being recorded, and you'll be emailed the link afterwards. You'll also be able to share it with others via our YouTube channel.
A little bit of housekeeping first: you'll see the screen as it is at the moment. Please familiarize yourself with the Q&A button on the screen because that's where you can put your questions as the event progresses. We'll get to those when we introduce our panel at the end.
We can't hear you, so don't worry about that; we can't see you either, so just sit back and enjoy. Do move around as you need, and please know that when we come to the questions and answers, we can't offer any tailor-made personal medical advice.
This webinar is one of three years, as part one, and they're all about arthritis. We're delighted and also very fortunate to have Associate Professor Tasha Stanton from the University of South Australia to present for us today. She works at the forefront of arthritis research, so get your questions ready for her. This webinar and the one next week will be live for you to watch, and then the third one will be pre-recorded. We'll aim to answer any questions that we haven't got to in these first two, so keep an eye on your inbox for that one.
The presentation today will be followed by a question and answer session, during which we'll also be joined by Celia, who lives with arthritis herself, and healthcare professionals Olivia Buxton and Andrew Cuff.
So, all of that said, I'm delighted to introduce Associate Professor Tasha Stanton with her presentation. Over to you, Tasha in South Australia.
Tasha: I'll just take a moment here. Yes, thank you. Can you see my slides okay there?
Yes, hello everyone! Thank you so much, and I'm really excited to join you today, particularly because Manchester has such a special place in my heart. Quite a few years ago, back in 2016, I visited the UK for a while and had about five or six days in Manchester, and I fell in love with the Christmas markets. I went to Mr. Thomas's Chop House, which was amazing, so I'm just really excited to be part of this event, given that it holds such a special place in my heart.
So, my talk today is going to be about flipping arthritis, and I'm really going to direct my talk towards those of you who have osteoarthritis. I know there might be clinicians or family members that might be joining as well, and all of this will be relevant to you, but it will be framed towards those who have lived experience with arthritis.
In my talk, I'm going to be referring to knee osteoarthritis a lot because that's my area of specialty, but please know that all of this information applies to osteoarthritis in other areas of the body as well. Now, finally, some of the things that I talk about today might feel quite confronting or hard because they don't jibe or they're not consistent with what you've heard before, perhaps from your healthcare practitioners or doctors. I just ask you to listen with an open mind, as many of the things I'm going to be talking about today are really new science.
To start, I want to share some of my disclosures so you know where I'm coming from and the things that might influence what I think about this area. I do receive payment for lectures like this on pain and rehabilitation, and I've also written a book about osteoarthritis, and much of that information I'm going to be presenting today. I also receive royalties for that and have received research grants and fellowships from numerous different agencies.
So, without further ado, I'm going to raise the idea that we actually thought that we knew everything about osteoarthritis—that we had it sorted, we had it covered—because we know what it is. We know that it is this degenerative disease of the joints. The best part is we can easily diagnose it. If we chuck people into the scanner, we can see it on the scan; we can see changes in the joints, and we know how to treat it.
So, we know that there are all these things going on, meaning we have to do our best to stay moving, do our best to stay strong, to make sure our joint is aligned, and try to keep our weight down so that we don’t have very much load and forces through that vulnerable joint. But, ultimately, we're probably going to go downhill, and we're probably going to need to have surgery to kind of cut out the bad bits and replace them with a new shiny knee.
Is that true? Do we know? We say we say this about this condition, and I want to challenge you that actually we might not, but that’s not a bad thing; it’s a really good thing.
So let's look at some of these things. This idea that we can easily diagnose it—we know we can see all the changes on scan, so we're fine; we know what's going on. Guess what? Diagnosis is not as straightforward as we thought.
If we take people who are not injured and who do not have any knee pain at all, and we check them into the scanner, up to 43% of people will show osteoarthritic changes on MRI but they have no pain. In fact, it’s been findings like this that have had different medical bodies suggest that having scans or MRIs might not be as important to the diagnosis of osteoarthritis because many of the clinical symptoms that occur—things like pain with activity, different challenges with various functions—those features are actually the most important things to know anyway.
So, we might not need many of these different scans. There’s also this idea that if we know how to treat it—if we cut out that degenerative knee and we replace it with a shiny brand new one—everything should be fine. Yes, total joint replacements actually help a lot of different people reduce pain and improve function, but if we look really carefully at the literature, actually the outcomes are not as good as we might think.
If we think that the only problem is the joint, because if we look at people over the long term—about 10% to 34%, depending on the study—have unfavorable long-term pain outcomes after they’ve had a total knee replacement surgery. Fifteen percent of them are still having moderate to severe pain two to five years after surgery, and this is really not infection; this is really no problems with the prosthetic that’s been put in, and they’re still having pain. So it suggests we might not actually know as much as we think we do.
If we look to what people with osteoarthritis have been told and what they think, it’s actually really consistent with the story that I just told you at the start. This is qualitative research asking people with osteoarthritis about their experiences, and many of them reported that they have a wear-and-tear disease. It's a disease they’ve overused their joint; they’ve lost their cartilage so that their knee is bone on bone, and that’s why they have pain.
Together, this overused, worn-out joint that has no cartilage left is vulnerable. They also hold strong beliefs that, yes, it's going to get worse over time, so it’s probably best that this is the best it’s going to be now, and it’s going to continue to decline. Because there’s this vulnerable joint that’s going to get worse over time, gosh, it makes good sense, doesn’t it, that we need to be a bit careful about what we do?
Because if wear and tear, if overuse is what's causing this problem, then actually loading my knee further by doing activity might not be a great idea. Yes, yes, yes, I know that all the clinical practice guidelines suggest that exercise and activity are good, but not for me because, for me, I don’t have any cartilage left—surgery is my only option; I need to replace that damaged cartilage, or I need a new knee.
If we look a bit deeper at what people think about exercise, these are some quotes from people with osteoarthritis, and they might ring true to you: "It seems like common sense that if you’ve got a deterioration in the joint, like which arthritis is, then the more you do, the more it’s going to get worn. You know I wouldn’t have thought it’s something that would get better with practice, you know, with exercise."
Or this one: "If it’s your bones that are grinding together causing that much pain because there’s wear and tear, how’s the muscles above or below really going to help?"
These are completely valid things to think because I would argue that advice to move, advice to exercise, advice to do physical activity makes absolutely no sense unless one first understands that osteoarthritis is not a wear-and-tear disease of the joint. Ultimately, that is what the new science is showing us.
So if we look back at what people with osteoarthritis have been told and what they think, many of these things are actually myths and misperceptions. What I’d like to do today is to explore some of the research that’s behind why we think these are myths and misperceptions. I think one of the biggest ones is this idea of wear and tear—that the more we do, the more we damage the joint.
One of the things I think is most commonly told to people when they have a diagnosis of osteoarthritis, certainly from the work with people living with arthritis that we’ve done, is that when they go in to see the doctor, the doctor will say, "Look, you need to lose weight because if you lose weight, it's actually better, because then there’s going to be less load, less force through those damaged joints, and that’s going to be helpful with your pain."
But this sort of presumes, doesn’t it, that it’s only about what’s going through the joint? I actually want to explore this myth a little bit further because what we see is that weight matters, but it’s actually not quite how you might think.
If people have a higher body weight, but it’s due to higher levels of body fat, that is associated with progression of osteoarthritis over time, so there’s increased loss of knee cartilage over time. But here’s the kicker: if you have higher body weight, and it’s because you have more muscle, more lean mass, that is not associated with progression of osteoarthritis; it stays the same, and in some cases, there might even be a reduction in knee cartilage loss over time.
So this shows us that it’s not extra body weight that contributes to progression of osteoarthritis and damage to cartilage; it’s potentially extra body fat. We see that there’s support for this—the idea that the amount of body fat that we hold might matter because obesity actually predicts the progression of hand osteoarthritis, which of course are not weight-bearing joints. We’re not looking at load through a joint when we think about hands.
So the available evidence doesn’t support kind of a biomechanical description of wear and tear, where if you weigh more, there’s more load through your joint. Well, no; it actually matters how your body is made up. The newest research we’re looking at shows that obesity or having higher levels of body fat—in what it actually does—is it increases inflammation, and inflammation can play an important role in the progression of osteoarthritis as well as in pain.
I’m going to come back to that in a little bit. So that’s one aspect of wear and tear—this idea that it’s only load that matters. But there’s another feature of wear and tear where we think because we’ve overused this joint and it’s all worn out, we have no cartilage left, it’s bone on bone, and it’s only going to get worse. Loading, things like that, are going to make it worse.
So the idea that your joint is bone on bone, that cartilage is damaged or non-existent, movement is going to be bad. Let’s challenge that myth a little bit because we actually only think of cartilage as changing in one direction—getting worse.
Cartilage is that lovely lining on the ends of your bones, and particularly in the knee joint, you have nice, big, thick cartilage across lots of surfaces of your knee joint. When we look at the literature, we see that cartilage isn’t a static, unchanging thing; it’s responsive; it changes, and it actually loves loading.
Because if we look to astronauts who go up into space, they’re not loading their joints at all, because they’re in microgravity. When they come back to Earth, guess what happens to their cartilage? It is thinner and it’s less healthy. So we actually see in the absence of loading a joint, the cartilage does worse.
Then we look at the opposite example—the marathon runners. From every other model, if you’re doing that much, you should be wrecking your joints. I mean, sometimes we do see in very, very high-level professional athletes that do crazy amounts—they can hurt their joints.
But if we look to the average marathon runner, interestingly, they often have healthier cartilage than people who are sedentary or who don’t do very much activity. So in this case, it suggests that actually loading is kind of a good thing. If we look at the physiology—so how cartilage actually works—we realize and understand that cartilage doesn’t have a blood supply.
So it gets its nutrients through compression and loading; that’s how it gets fed. When we're walking, we're rhythmically loading and compressing our joints—that's nourishing our cartilage. We also know that in cartilage, you have these specialized cells that are called chondrocytes. They’re good value; they make collagen, which is tough stuff, and they make aggrecan, which is sticky stuff, and that’s the basis of what cartilage is.
These chondrocytes love loading. If you load up chondrocytes, they go out from the chondrocyte to other areas of the joint and can actually go and target different damaged areas of cartilage.
So instead of saying wear and repair or wear and tear, what we probably should be saying is move to improve. The more we load, the more we can help the health of our cartilage—or rather, the more we reload, the more we help our cartilage.
Now, you might be thinking, "Alright, smart guy, if cartilage loves loading that much, why then does it hurt when I move?" If it’s hurting when I move, shouldn’t I be worried about that? Because isn’t that telling me that I’m doing more damage to my knee?
Let’s explore that. The available evidence suggests no; it’s not doing more damage, and I’ll explain why. We know that there are changes to the pain system in people with osteoarthritis that are a bit like the cat in this picture here, who’s doing a huge jump when there’s a cucumber.
These changes to the pain system mean that that the system itself is overprotective or oversensitive. So if we look at the data, we see that people who have painful knee osteoarthritis are more sensitive all over the body.
So these are findings where we do pressure pain thresholds; we basically press on the skin, we press down, and we stop just at the moment it starts to hurt. The amount of force we apply is the pressure pain threshold—how much pressure it takes to hurt. You can see here that unsurprisingly, people with knee OA—they’re in the red bars there, and if we press on their painfully yes, they’re much more sensitive; it’s much less force before pain comes on than a healthy, pain-free control.
But if you look at the other data, this also occurs if you press at the thumb, and it also occurs if you press at their trapezius muscle. So it’s all over the body. The question is why.
We’re starting to understand that it’s a few different things. First, I talked to you before about this, and it comes back to inflammation. But before we get too deeply into inflammation, I want to just do a quick review or a quick delve into how our pain system actually works.
So if we step on a thumbtack, like in the bottom picture there, when that happens, specialized receptors in our body—the technical term is called nociceptors—what we often call them is danger detectors. Those specialized receptors activate, send a message up the nerve to the spinal cord, and send that message up to the brain.
You have those exact same danger detectors in your knee. So if something happens, let’s say you have—maybe you’re doing too much one day, doing something too quickly—the danger detectors activate and send a message up to your spinal cord and then to your brain.
Now, a really important part of this to understand is that the message that’s being sent up to the brain from your knee is not pain; it’s actually a message about what’s going on in the knee saying we have potential danger or threat going on here because there are a lot of different contributors and types of information that tell us about danger or threat.
Ultimately, what we’re trying to determine is, do I need to be protected? Because pain is a great protector. First of all, it catches our attention, doesn’t it? It stops us from doing things; it makes us change behavior—all of these things can be protective.
So we’re considering this danger message from the knee, but also all these other things are used in making that decision and determining whether or not we feel pain. First of all, what I'd like to focus on is what happens to this danger message in people who have knee osteoarthritis.
So here’s where I’m going to come back to this idea of inflammation. We’re starting to understand that osteoarthritis is not just a disease of the joint; it actually involves increased body-wide, or the technical term is systemic inflammation.
So higher levels of inflammation—this is like when you have the flu; you don’t feel great. You feel sluggish. All those areas that you’ve hurt 10 years ago or 20 years ago all of a sudden start to hurt and feel painful again.
So inflammation—as we get older, actually, we begin to have higher levels of inflammation; it is just something that occurs. For people who have osteoarthritis, they often are 50 years and older. It’s sort of got a system that’s set up to have higher levels of inflammation right away.
I referred to this before, but also when we have higher levels of body fat. You know what body fat does? It’s so tricky, man; it basically produces a special molecule called an adipokine, which increases inflammation.
So you have different parts of your body that are producing these things that increase inflammation, but also you can have changes in your gut microbiome—so all the different bacteria and things that occur and live in your gut. What’s interesting, and what many people don't realize, and I certainly didn’t realize until probably about five years ago, is the extent to which your gut microbiome communicates with your blood circulation.
So when things are off, what it actually does is can, through communication, increase your body’s inflammation, and that includes things going on in the knee. So all these things increase inflammation.
Now, let’s look at what it does to that danger message. Let’s say you’re walking up a set of stairs, and those danger detectors in your knee are being activated by that mechanical force as you're going up the stairs.
Now, let’s say that arrow there is the size of the message that’s going up to your spinal cord based on how many danger detectors have been activated. Now in the presence of inflammation, the danger detectors are more sensitive, and they also call in their friends, so way more of them activate than they normally would.
So your danger message goes from this to this without any change in your knee at all, merely in the presence of inflammation. Now let’s look at what happens at the spinal cord.
So that danger message goes up to the spinal cord. Now in the presence of inflammation, the nerves in your spinal cord are more sensitive, so a danger message coming up is more likely to activate the message going up to the brain.
But they also bring in extra friends, so you get this message that goes from this to this size without any difference going on in the knee joint at all, merely because of inflammation. That is sent up to the brain.
We’ve gone from a danger message like this to a danger message like this with no change in your joint at all. What’s intriguing is that all of those other factors that I listed on that previous slide can mean that the importance of that message can be amplified when it gets up to the brain.
So, you can see this large disconnect or change in the size of the danger message, which means that sometimes how much pain you feel is not necessarily telling you solely about what’s going on in the joint, but it might reflect how much inflammation is in the system.
But, friends, it's more than that. Our nervous system has natural brakes and accelerators. The brain sends down communication to the spinal cord, and this communication can either make the spinal cord less sensitive—so it’s actually harder for that danger message to get up to the brain—or it can make it more sensitive so that it’s much easier, and that message gets bigger and bigger.
Now, here’s what we know, based on the research in this area: the brakes are impaired in people with osteoarthritis. They are more than—unable to make that system less sensitive, and it’s about two times worse than people who don’t have painful osteoarthritis. But it’s not only that the brakes are impaired; the accelerator is working too well.
So what do we get? We get a situation where you’re way more sensitive. Even if we didn’t have any inflammation at all, if these systems aren’t working as well, what it means is that the size of that danger message getting up to the brain can be way bigger, just because these systems aren’t working well.
So again, it can make sense why how much we hurt might not always reflect what’s going on in the joint. So these changes to your neuroimmune system, and these changes that occur in painful OA, it’s a little bit like road rage—but when you’re hungry.
If you think about when you get cut off when you’re driving, you’re quite annoyed and you’re a bit mad, and you might give a little toot-toot of the horn. But think about if you’re starving hungry, what do you do if you get cut off? It’s a blaring horn; it’s probably yelling; it might be swearing.
Then, actually, you’re still annoyed by the time you get to the next light, and maybe you’re waiting to turn, and someone didn’t pay attention; you’re blaring the horn again—“Get going! You had one job!”—and maybe it’s not even limited to driving; maybe you see someone hesitate when they’re trying to cross the road, and that means you’re going to have to wait longer. Blare on the horn again.
You can’t control or reduce that reaction because you don’t have any food; you don’t have any inhibition. There’s nothing there to make the system less sensitive.
So this amount of pain that you experience—all these different changes—they explain why that amount of pain isn't just a linear or a direct reflection of the amount of things that are going on in the knee. And that’s actually a really good thing because we can change these things!
Now, this is a lot of big concepts. Clinicians—we would learn this over probably three months, maybe a year. I want to present this in another way that’s a bit more visual.
So this mountain that I show here—this is the amount of activity that someone is doing. If we take a healthy person without any pain at all, if they did a crazy amount of activity, they would hurt themselves.
We all have a certain tissue capacity, and if we push too hard, we will injure ourselves. So if I tried to run a full marathon tomorrow, I would undoubtedly injure myself because I haven’t trained for a marathon.
However, what’s really cool about our systems is that we have to protect our pain line. We have a safety buffer where if we have sufficient time, pain comes on often before we injure our tissues.
If you think again about the pressure pain thresholds that I was talking about, that’s a perfect example. We’re pressing into the skin until we feel pain. But when we first feel that pain, we’ve not damaged anything; we’ve just activated those danger detection systems, and we decided, “Yep, that’s sufficient enough that I should pay attention,” and it hurts.
Now, in a person with osteoarthritis, there are changes to the tissues; there are changes to the cartilage and changes to other tissues of the joint. It means, then, that their tissue capacity is probably less.
So for most things, it would take less of a big physical effort to cause injury. However, thinking about all of those changes that I spoke about—the change with inflammation, the changes to the brakes and the accelerators of the system—it means that that safety buffer is much bigger.
So the system itself is becoming oversensitive or hypersensitive or overprotective. Now, the important part of this means that—think about what happens if we start to do a big walk and we start to do that amount of activity, and we start to push into that safety buffer and we feel pain, but we’re nowhere near tissue capacity. We’re just pushing into that safety buffer.
So it means that when we’re moving, it’s actually okay to feel sore. You’re safe; you’re nowhere near tissue capacity, and that can be a really helpful thing, actually, to understand.
Now, another—I talked about the inflammation and the changes in our brakes and accelerators. There are also a lot of other things that can contribute to that safety buffer size.
Our beliefs, fear, anxiety—if we don’t get any sleep—all of those things dynamically alter the safety buffer. So if we go back to this overall figure that I showed you before, we’ve talked about what happens to the danger message itself, but it’s really good to remember that all of these other things—knowledge, environment, comorbidities, beliefs, expectations, past experience, thoughts, feelings, fears, stresses, sleep—all of these things can provide relevant information about whether or not we need to be protected.
So pain isn’t just a readout of what’s going on in the tissues. But instead, the science supports that we have a dynamic system, and it adapts and updates all the time based on the available information that’s around us—for a person coming from our body—in the environment that we’re in and in the society that we’re embedded in.
This dynamic system is about protection. Do I need to be protected? Do I need to feel pain? Do I do I need something to draw my attention? Do I need something to change how I move or how I behave?
So it’s considering all the available evidence of danger and weighing it up against all the available evidence of safety to determine, “Do I need to be protected?”
Now, the cool thing about this and what it means for you is that based on this idea, anything that suggests you need protecting can increase pain. Maybe hearing something from a health professional or seeing something on TV—“You better not do that; you might injure yourself”—anything that suggests you need protecting can reside up here as electrical impulses and contribute to your feeling your need to protect and feel pain.
But also, anything that suggests you don’t need protecting can reduce pain. This might be a supportive, helpful clinician; this might be learning some of these things today and understanding, “Actually, why does my joint hurt when I start to move?” But actually it’s okay; you’re sore, but you’re safe.
So all of us have a unique balance of what we call danger in me’s (DIMS) and safety in me’s (SIMS), and these can come from lots of different places.
So it can be really helpful to think about the different contributions in your own lives. For example, this can come from things that you see. A danger could be looking at your knee x-ray if it makes you feel anxious and worried; a safety might be actually, you know, feeling how strong your thigh muscles are, knowing that you've got a nice strong leg. That can be a safety thing you do—knee exercises.
Depending on how you view that, that could be a danger, but I’ve got to start there because, depending on how you view that, things like knee exercises can also be a safety in me.
It might be things you say. Do you say wear and tear or do we replace that with wear and repair or move and improve—strive and thrive? It could also be things that we think.
If we think, “You know, surgery is inevitable,” that for some people can be a danger, or thinking, “Actually, there are many ways to improve my OA,” and I’m going to come back to this in the end of my talk, but that feeling of hope and of possibility and of change is really important and can be a safety.
Places you go—a doctor’s office, that smell, the lighting—that could be a danger in me. Going to a dance class with your best friend can be a safety. The people that you work with or that you see could be a danger; it could be an out-of-date health professional, someone who doesn’t listen, someone who doesn’t hear you.
An up-to-date health professional—someone who’s on your side and working through this with you together—can be a safety. It can be what you're sitting at—are you feeling depressed and anxious? That could be danger. Happy, happy, and optimistic can be a safety.
One thing that I’d be really interested to have you think about, when you place it whether it's a danger or a safety, is many people that I know have had their surgery delayed due to COVID and the backlog that’s occurred.
The question is, do we view that as a barrier that’s awful and that has stopped us from doing things, or do we consider that delay as an opportunity?
What I’m going to talk through next is treatment that has actually been shown to delay or prevent joint replacement surgery. The thing is, I don’t want to make it sound and seem that surgery is a bad thing for everyone; it’s not. Sometimes it’s the right decision.
But oftentimes, we don’t know that until we try to see if we can get things under control through other ways that don’t involve surgery. I might suggest we could frame this as something that’s a safety because you have a window of time to try this out. Worst-case scenario, you are fitter and healthier before you undergo surgery; best-case scenario, you might not need it. You never know where you might go—you might be pleasantly surprised.
So our steps to OA recovery—there are actually three key ingredients, and a bit like making bread where you need flour, you need water, and you need yeast all together to actually make bread, similarly, you need all three of these things together to really have the most impact you can feel.
The first key ingredient is increasing knowledge—some of the things that we’ve talked to through today—that’s already increasing your knowledge. The second is increasing activity, and I'm going to go through that in a little bit more detail. The last is decreasing inflammation.
I strongly believe the focus should not be on weight loss; I think it should be on many different strategies to overall decrease inflammation levels within our body.
I’m first going to talk a little bit more about increasing knowledge because I’ve given you some knowledge about knee osteoarthritis now, but it may not make sense as much why this matters so much.
Because actually, your knowledge and beliefs about osteoarthritis, they really do matter. If we look to the science, we find that the knowledge and beliefs about your own body can influence the pain you feel. This was a study where they were getting healthy volunteers, and they were zapping them with a laser, but they first did a skin assessment to see that it was okay to zap them.
They marked out the areas that were completely fine—like, “Yeah, it’s completely safe to get the laser zap here”—but then they also noted some areas that should be okay, but they might need to be a bit cautious and just watch.
So, areas that are not quite sure that it’s safe—important to know, skin assessment entirely false. So in all areas of the skin, it’s totally fine and safe to receive the laser zap. The only thing being manipulated is a person's perception of how safe it is.
So then when they zapped people with lasers in these different spots, what they found is that when they zapped that spot where people were not sure if it was safe, the laser zap was more likely to hurt, and it was more likely to hurt more as compared to the area when you zapped that people believed was totally safe.
This tells us that things hurt more when you aren’t sure that they’re safe. That makes sense, doesn’t it, if we think about danger—the contributors to danger, but also this belief that I’m not sure that this is safe.
This may have real implications for feeling pain during movement and exercise. If you have a fear of, “I’m not sure this is safe for me,” your body is already on high alert.
Now I just want to pause here for a minute because, like, how on Earth can knowledge and beliefs actually change what I feel? I don’t know about this. Well, I’d like to give you an example of how what we experience can be profoundly shaped by other information that’s available.
I’m going to show you a video. There’s a guy in the middle of the screen, and on either side of him, there are words. I want you to read the words that are on the left-hand side of your screen. Read them out loud to yourself. I’ll say them as well, and then I want you to listen to what you hear.
So I’m just going to get this video running. I’m going to click on it. It’ll just be a moment. [Video plays.] Green needle.
What word did you hear? Hopefully, what you heard there was "green needle."
Now I want to play the exact same video again, but I want you to read the words on the right-hand side of the screen. Brainstorm.
You will only hear the word that you’re reading. Isn’t that amazing?
So basically, when you read that word, you’re priming your brain to expect a certain sound pattern. When you get this sound that’s pretty low quality and it’s noisy and is a bit ambiguous, your brain does a best fit between what it expects to hear and what’s actually coming in, so you only hear the word that you’re reading.
Isn’t that incredible? It shows because all of our sensory information coming in from our body, there’s a lot of it, and it’s really noisy.
So what we think and we believe helps sample the information ironically to what we expect. So if we expect things to go really poorly, oftentimes we prime our body to experience exactly that.
Because it determines how we sample incoming information, we are complex beings. So to me, what this also tells us is that there’s real relevance between the words that we use and the words that are said to us in terms of osteoarthritis.
And I would like to go through some words that I think are really helpful and we need to just get rid of—we need to debunk and push away. There are some unhelpful words, and I’ve referred to some of these before—things like "bone on bone" and "wear and tear."
These are dangerous; they tell us your body is damaged, it’s vulnerable, it’s fragile, and I would argue they’re not as evidence-based. Because if we look at x-rays, it can look like things are bones touching, but actually, you always have this fluid in between those joints.
You have this luscious lubricant called synovial fluid; it is slippier than anything we’ve ever created—better than Teflon. Nothing sticks. It’s slippery as, and it’s always there.
So why aren’t we talking about that instead of wear and tear or bone on bone? In terms of wear and tear, why don’t we talk about the fact that loading can stimulate those chondrocytes to move?
So maybe wear and repair, or even better, strive and thrive—move and improve. Because all these things are telling us our body is resilient and robust. They’re giving us safety.
Scans are also another big thing. You may have been told unhelpful words in relation to them. You might have heard something like this from a health practitioner: "That’s the worst x-ray I’ve ever seen," or "You have the knees of a 70-year-old."
If you’re 90, that’s a wonderful compliment! But the trouble is that usually gets told to a 30, 40, or 50-year-old, and it’s absolutely terrifying. A lot of times, I think clinicians are meaning well with this. They’re almost trying, I believe sometimes, to validate: “Well, no wonder you’re hurting so much; this is the worst x-ray I’ve ever seen.”
But first of all, it doesn't quite match with what we know is going on in osteoarthritis that we talked about before. Also, it gives you this danger in me: "You should be worried at how bad this scan is."
Even a health professional that’s seen so many scans thinks this is bad, and it’s also things saying—saying things like “this isn’t necessarily accurate” because we do know that exercise, x-rays, and scans don’t tell us very much about the amount of pain you feel right now, the amount of pain you’re likely to feel in the future, or how much activity you can do.
Hearing things like this might make you feel angry, and that’s okay! Many times scans can be important in some cases, and I'm not saying that what is going on in the joint isn't important at all—it definitely is.
But just remember, scans aren’t good at capturing the complexity of everything. Remember all those changes that I spoke about—the inflammation, the nervous system changes? We can’t capture that on a scan, so it’s inherently an incomplete picture.
Think about it a bit like looking at a picture from a family reunion. Because everyone’s smiling, we presume everything went beautifully—when it’s very unlikely that was the case. We just had a picture in time, and a scan is a bit the same.
What they do tell us about, actually—and interestingly—is findings that are actually really quite common and normal with age.
A lot of the things that are reported on scans sound abnormal or scary—like degeneration or degenerative changes, or even meniscal tear—actually, a lot of them are related to age.
So people of the same age—one with very little pain or no pain at all and one with quite a bit of pain—many of them will have the same findings on a scan, and they just get more and more common as we get older. So some of these findings are a little bit like wrinkles but on the inside.
That can be really helpful to know what things might be normal on a scan. Instead, so instead of saying things like, “The scan is terrible,” we want to say, if it’s appropriate, “The scan changes are a bit what I would expect."
We can think of them a little bit like wrinkles, but the key bit is these changes can be normal, but they don’t tell us what you’re capable of.
We see people who have maybe very scary-looking scans, if we didn’t know anything about them, they don’t have any pain, and they’re actually incredibly active, doing a lot of things.
But there are also sometimes not helpful words about your future—things like “Your joints wear out as you get older,” or “You better get used to it; this will be here for the rest of your life.”
They're saying you’re stuffed; it’s just going to get worse; “You better be careful how much you do.”
This is an important one to challenge because this isn’t the case. We are all bioplastic.
What that term means is that our systems, our tissues, they can always adapt and change, even in people who have painful osteoarthritis— even in people who are 90 and above. This bioplasticity—this changeability—never stops.
It might slow down as we get a bit older, but it’s always there. So this is a message of hope. This is saying our systems are designed to adapt and change. All we need to do is we need to give them the right push or nudge to then make them respond and have to change.
Some ways and examples of bioplasticity can be when we lift weights—that’s our push or our nudge to the system. You get sometimes larger muscle size; you get greater strength.
If we practice a test, we get quicker reaction times—bioplasticity. If we do weight-bearing exercise, guess what? You get healthier cartilage, and you get increased bone density—bioplasticity.
And actually, our pain and our immune systems are bioplastic as well; they can change, and that’s really important.
So the next of the key ingredients is really increasing activity. If we look at the research that’s been done in this area, exercise and activity are one of the best treatments for OA because it is a big push or nudge to your system.
It induces this bioplasticity—it makes your system adapt in response to this increase in movement, and this is really key.
Learning more about osteoarthritis— that also is a push to your system. This is a physical, a movement push, and it has a lot of really general and important benefits.
It can increase your confidence and your self-efficacy, or your feeling of your ability to do something. It has been shown to generally improve mood and quality of life.
What people may not realize is that when we get the dose right, how much you do, it can decrease inflammation in people with osteoarthritis. Well, that's handy!
It can also improve the brakes of the pain system, so it can help make things less sensitive.
So two different things that are helping to make things less sensitive—exercise improves cartilage health, even in people with osteoarthritis.
If you happen to start to lose some body fat—remember body fat can also contribute to inflammation—so you can reduce inflammation on that front.
We have found, also, that when we slowly but surely increase exercise over time, it decreases the overprotectiveness of the pain system, even in people who have what we might term severe OA.
Critically, if we pair education with exercise, we can take advantage of the fact that increases in exercise or activity improve brain function as well as learning and memory, and when you have a lot of pain, actually, you feel foggy; it can be hard to learn, to remember.
So pairing these together is a really good thing. Now, I want to come back a little bit more to this point—this idea that slowly but surely increasing over exercise over time matters, and I want to come back to the diagram that we used before.
This is where we showed an increased safety buffer in people with OA. Now when you start to increase exercise and activity levels slowly but surely over time, it gives your tissues a push and requires them to adapt.
It can increase your tissue capacity. Here I’ve put it back to normal; I’m not sure they would actually make it completely back to normal but it can improve.
We also see that when we slowly but surely increase exercise over time, what we can also do is start to reduce the safety buffer. Remember I talked about how exercise can reduce inflammation; it can improve the brakes of the pain system.
If you’re not feeling more anxious and nervous and scared, if you’re sleeping better—all of these things can reduce that safety buffer.
What it means is that you can do more and with less pain, and that is a critical outcome. We’ve tested this idea of education and exercise in a feasibility study, and we were looking using a walking program to increase physical activity, and we found really promising results.
We’re currently actually testing these in a really big randomized controlled trial, so hopefully we’ll have those findings soon.
But just to show you that we have evidence to suggest that slowly but surely increasing matters, I think one of the key things—and it’s actually what I’m going to touch on in more depth in my next lecture—is that it can be really scary to know, “How much should I do? How much is safe for me?”
So this is where it's really important to work with someone to help find what we call your sweet zone.
It’s the amount of activity that’s not too little; it’s not too much; it’s just right. So if you’ve tried exercise before and thought, “Ah, all it does is make my knee feel worse,” you might have been in the too much zone.
Or if you did exercise before and you thought, “Oh, I see no benefits whatsoever,” you may have been in the too little zone.
I’m going to come back to this concept because this is the idea that helps you know that you feel quite certain that what you’re doing is right for you.
Now, last but not least is decreasing inflammation.
The three biggest ways that you can decrease inflammation—well, one of them I’ve spoken about already, haven’t I? And that’s increasing your physical activity levels. That can reduce inflammation when we get the activity level right—it’s a huge thing.
Now, I’m not an expert in diet, but the general rule of thumb in decreasing is eating processed foods—things that come pre-packaged in wrappers or from a takeaway shop. Decreasing the amount that we have—and that doesn’t mean never; it just means in moderation.
Trying to increase some of the green leafy vegetables, berries, turmeric, ginger, oily fish like salmon—a Mediterranean-type diet—can be helpful in reducing inflammation.
What people might not know is that, actually, what we feel and think—negative or positive affect, as we call it, “I can” or “I can’t do something”—that can influence inflammation.
Feeling helpless and negative about things actually can increase inflammation. So here’s where—as we understand more about osteoarthritis, and maybe we feel like, “Yeah, I’ve got a way forward,” and actually I’m not as worried that I might hurt myself or do something bad—I can change; I am bioplastic.
That gives hope, and we can also then take advantage in terms of reductions in inflammation.
So I would argue that advice to move makes sense when one understands that osteoarthritis is a dynamic low-level inflammatory process; it evolves. Nervous system, immune system, gut, diet, adiposity, mind, past experience—the environment, joints, that person—and all of these aspects of the person—all of this is bioplastic; it can change.
So in summary today, I hope what I’ve convinced you is that osteoarthritic pain is actually quite complex.
This sounds like it’s a bad thing, but it’s actually a good thing because it means there are many different contributors to pain.
So we have many different targets for treatment, and we are bioplastic, and exercise and education are some of the best ways to retrain an overprotective pain system, to reduce inflammation, and really encourage cartilage health.
And we all are changeable. Wear and tear? Throw it out. Move and improve—that’s our new lexicon.
And there are these three key ingredients to recovery: increasing knowledge, increasing activity, and decreasing inflammation.
So we’ve had a lot of information, but on this note, I want to wrap up, and I believe we’re now going to be joined by a panel discussion.
So thank you so much for your time and your attention.
Felicity: Thanks very much, Tasha. That gives us loads to think about.
We will get to your questions very soon, but first of all, I want to introduce our panelists. We know Tasha from South Australia. We also have, let me get my order right, Celia. Do you want to introduce yourself?
Celia: Hello, my name is Celia Borland, and I’m a retired social worker, and I live in Edinburgh. I’ve been living with osteoarthritis with persistent pain in my left hip for about three years now. Initially, I really struggled with the pain and was very cautious about activity. I was going to see my GP and having an x-ray, which showed that my left hip was very severe osteoarthritis and that my right hip was severe to moderate in arthritis.
But she suggested I get lots of exercise and maybe see a physio. So I went to see a physio who introduced me to flipping pain before we even started talking about exercise, and that has made all the difference to me because I’ve really learned about flipping arthritis and the understanding of my pain and condition.
What happened is that, although I do take some drugs, I learned to transform my life by going out walking, which was something I’ve always loved to do but had retreated from for over a year, just being very careful and resuming all the things I loved into my life as I began. It became worth it.
That’s me!
Felicity: That’s brilliant! Thanks very much, Celia. Olivia, I’ll come to you next to introduce yourself.
Olivia: Hello! My name is Olivia. I’m an MSK physiotherapist within Rochdale, and I work every day with osteoarthritis patients. I have a special interest in what flipping pain is doing in terms of increasing the knowledge around osteoarthritis and promoting the move and improve aspects to it, trying to get patients back to their normal life, really.
Felicity: Brilliant! And finally, I’ll come to you, Andrew, to introduce yourself.
Andrew: I’m Andrew Cuff—I’m a consultant physiotherapist by background and the head of MSK for connected health. My role is predominantly clinical and working with patients with arthritis, but I also have some oversight in terms of our pathways, our models, and ways to innovate and improve arthritis care for the benefit of patients.
Felicity: Excellent! Thank you very much. So what I will say in advance of launching into our questions here is our next webinar will be heavily focused on physical activity and how you go from perhaps not doing as much physical activity to doing what you want to be able to do.
So if you’ve asked a question about activity, it may be that we come to that in the second webinar. But we’ll see what we get through today. A couple of questions about diagnosis.
Let’s start with because there might be people watching who suspect they have arthritis but haven’t been formally diagnosed. So let me come to, let me come to Andrew as a clinician. Who can diagnose osteoarthritis, and do you need to see a specialist to get that diagnosis?
Andrew: Any healthcare professional can diagnose osteoarthritis, and it doesn’t have to be a specialist; it doesn't have to be somebody who only treats osteopathic joints. A general practitioner or a member of the primary care team—a nurse, a therapist—will be familiar and should be familiar with how osteoarthritis presents and be able to make that diagnosis.
It’s really key when you think about the diagnosis of osteoporosis, and Tasha touched upon this in her talk, is that it is a clinical diagnosis. It’s something that’s based upon signs, symptoms, and impact.
It’s that kind of back and forth between what the person's experiencing and what the clinician is picking up that informs the diagnosis. It’s not something that is informed by x-rays. We can’t diagnose osteoarthritis on an x-ray in isolation, and that’s something that I think is really key with really balanced health professionals.
Again, Tasha touched upon this: not every professional kind of aligns with what the guidelines say regarding making a diagnosis. We definitely over-image and we definitely call out the wrinkles and gray hairs and put a diagnostic label on them, but it’s a clinical diagnosis based upon signs and symptoms.
Felicity: Excellent! Brilliant, thank you very much. A point to come to you on, Tasha, about cartilage. Someone just wanted to clarify, are we saying that cartilage can repair itself? Is that what we’re seeing?
Tasha: I think what we’re definitely saying within this is that we have evidence to suggest that it can positively adapt. I am not aware, and I would love to find this study within humans, but a lot of the studies that have looked at changes in cartilage through loading have typically used animal models such as sheep.
There have been long-term studies that have shown in humans—and we use MRI, and we look at a specific marker within cartilage that is thought to be a marker of cartilage health—and that shows that people who are active have, and these are people with osteoarthritis, healthier cartilage than people who are not active.
So we do have evidence that there is an improvement in that. What would be an ideal study that we could run is we would need to randomize people either to exercise or not and then measure various measures of cartilage health over time.
But the reason I feel quite optimistic about things like that is if we look—so this is not osteoarthritis, but if we look to other areas where they do really quite radical surgeries on bones, maybe due to a trauma accident or something has occurred where they basically have to realign the way bones work, the cartilage of your joints changes based on how something is loaded through the joint.
So we know it can adapt in those certain circumstances. My thought is, and I would suggest that certainly the evidence supports that when we have activity, we’re more likely to have cartilage health.
What the physiology suggests is that when we do have this loading, it creates the environment to be right for repair of cartilage. It’s quite interesting because daughter cells that come out of chondrocytes, they move really slowly; they’re not fast-trackers.
I think in terms of those things, these would not be changes that we would expect to see six weeks into an exercise program. They would be changes you would expect to see if you’ve been walking, walking, walking, staying good, and you might see these changes over one to two years.
So I think it’s an area we really need to look into, but the available evidence certainly suggests that activity and movement and loading are very beneficial for cartilage health.
Felicity: Excellent! Thank you very much. Olivia, there’s a follow-up question to the one I asked Andrew. Which I’ll come to you on: Andrew is saying it’s a clinical diagnosis. We’re looking at the person. Somebody is asking, “Do I have to scan to diagnose?”
Olivia: As Andrew has answered in the comments, we’re seeing it on a daily basis. People with osteoarthritis—many people who haven’t had it, had a scan; we’ve simply diagnosed them through their signs and their symptoms and what they’re telling us.
So yes, so many people come right into Rochdale service from self-referrals, from GP referrals, and they’ve kind of just come in with knee pain. They might not know that they have osteoarthritis or what’s going on there, which can also be quite worrying for them when you’ve just got this pain every day and you don’t really know what’s causing it.
So yeah, we look at the person’s whole life, really, kind of what their signs and symptoms are telling us, what their background about it all is—what their function is—and look at their clinical symptoms and then make the diagnosis off that.
That can be really helpful, as well, when looking at rehab and treatment for it and where to kind of go next because we really want to tailor it to that person and kind of meet their needs for exercise and how we’re going to manage it going forward.
So yeah, we don’t always need scans; it’s very much on the person. I always say treat the man, not the scan.
Because, like Andrew says, sometimes we can scan people, and it looks like the worst one ever, and they come in, and they go, “I’m pain-free; I have no pain whatsoever.” It does not necessarily mean that they’re going to be in pain.
So I like to treat the person, tailor it off the person’s needs and what they want out of life, and kind of go back to how they’re doing with it and treat them off that, really.
Felicity: Thank you very much. Celia, does that fit with your experience? You mentioned you’ve got signs of degeneration—up to quite severe degeneration on both hips.
What’s your experience with pain in either hip?
Celia: Well, that was the thing. I took this piece of paper that told me what was—it was on the x-ray—to the physiotherapist and said, “Look what it says; severe for both of them.”
He said, “But you’re not telling me that there’s anything wrong with your right hip.” I said, “No, you’re right; there’s nothing on the right hip.” He said, “Well, this is why we need to look at it in a different way.”
That’s why he introduced me first to physical exercise—before we even started talking about exercise—and that has made all the difference to me because I’ve really learned about flipping arthritis and the understanding of my pain and condition.
I learned that although I do take some drugs, I transformed my life by going out walking, which was something I’ve always loved to do but had retreated from for over a year—just doing very little, being very careful—and resuming all the things that entered my life as I began.
It became worth it.
Felicity: That’s brilliant! Thanks very much, Celia. I’ll get to talk about the surgery in a sec, but first, let’s talk about the pain science.
Tasha, probably a good one to come to here. Somebody’s asking: the sensitization of the nervous system that you mentioned, is that something that happens over time? Can it be reversed?
There's a question recently coming about tolerance of pain. Does that change? Does our tolerance of pain get worse?
Let's talk about the kind of that role within the threat and the nervous system’s perception of that.
I’ll let you go ahead with that first question, which was: does that happen over time, that change?
Tasha: It’s quite interesting because even if we experience an acute pain experience—let’s say we roll our ankle—sensitization of your nervous system occurs right away.
When you have that tissue injury, there are chemicals that go out that make your ankle itself way more sensitive. But not only that, the messages that go out to your spinal cord right away make everything in the spinal cord, going up as well, more sensitive.
So, even with an acute injury, it can happen really quickly. What we think occurs in osteoarthritis is an interesting one because we do think that there often are danger messages that are coming from some of these joints, particularly when you have higher levels of inflammation, and everything’s more sensitive.
So what that means is when we have that occurring quite often, that can cause that increase in sensitivity. And as long as there’s still stimuli going in, it can maintain it, and particularly if you have higher levels of inflammation paired with feeling really nervous, scared, stressed—worried—all of these different things that can activate pathways that go from your brain to your spinal cord that are the accelerators of your nervous system.
So yes, it can develop quickly, particularly in the presence of higher levels of inflammation. But the good news is, though, is that this can change.
So those graphs I showed are starting to get those slow, sure increases in activity levels over time that reduce that—that showed reduced sensitivity of the system.
Part of that we can measure with lab tests; we can also use functional activities, like one of the ones that we look at is we get people to do a six-minute walk, but we’re not interested at all really how far they can walk.
What we are interested in is how much their pain ramps up when they walk, and we see reductions in how much or how quickly pain ramps up when you’re doing a specific kind of stimulus to that joint, so you’re doing a walk, and that is used as a measure of what we call central sensitization or increased sensitivity of the spinal cord and above.
I think the good news is yes, all of that is changeable—in both directions.
Felicity: Excellent! Thank you very much. I’ll stick with you, Tasha, because there are a couple of questions about other things that we can change.
What can be changed first of all—deformities? When you’ve reached a point of your arthritis where the bones have changed and you can see, in this person’s case, in the hands and the feet.
Can that be changed?
Tasha: Oh, isn’t that a really good question?
In terms of hands, the truth is I’m not sure. Interestingly, there’s a lot less research on hand osteoarthritis. I really got to get on that because I think it actually is a really, really important thing to be looking at.
In terms of when there are deformities present, I think that there can be benefits seen from looking at other things that we might consider to be more physical type treatments.
So, it can be some people do find help with things like insoles or orthotics, but I would just, I guess, suggest that they’re not necessarily for everyone.
There was actually a very recent study that was out that was looking at, it’s called an offloader brace where basically it was for people who had, I think, deformities of their legs, so there was a lot of pressure on the inside of their knee and they used a specific brace to try to reduce that pressure that’s there, and people had benefit of that.
I think the challenge is, it’s not a one-size-fits all because even sometimes people that they have what might look like quite bow legs. You might consider that if you looked at an extra MRI, you’d consider that as quite a deformity.
Actually, if they didn’t have it their whole life, sometimes if they just reduce inflammation levels, despite the fact that they’ve changed none of those physical aspects, the pain reduces.
So I think we have some evidence that targeting various different contributors can matter. Probably one of the key things is being a bit like a detective and I think really backing up what Olivia has said here is treating—looking at those things for you as a person and looking at all the specific contributors that might be there for you in order to see what might work best.
Because I think that’s the hardest part; it isn’t a one-size-fits-all approach.
Felicity: Brilliant! Thank you very much. Another question which I think Tasha we’ll stick with you on—the diet side of things and the inflammatory side of things.
If someone’s living with lipoedema, so they have a higher level of body fat but related to lipoedema, that’s, first of all, that’s going to be difficult for them to change if at all possible.
We also know, even if you haven't got lipoedema, that living with a higher level of body fat is not—it's not a quick fix; it’s not something you can turn around very quickly.
What would be your advice for someone who’s finding it very difficult to change their levels of body fat with their diet?
Tasha: To me, I think that then is the key—that that’s not the only aspect of it. So even if body fat levels don’t change at all, changing the diet can change your microbiome.
So you can have changes in the balance of different things that are in your microbiome; you can have increases in the healthy ones, so to speak, and so that alone can have changes independent of body fat or body weight.
And so that can be really quite compelling in some people. Like, large changes in addition to that—even moving more, if we get that exercise level right, it does show that it can help have changes in terms of inflammation just by doing that exercise as well as increasing the brakes on the nervous system to reduce sensitivity.
So that’s I think comes down to this really interesting aspect that a lot of the research is showing is that it isn’t necessarily solely about how much activity you're doing. Like, there’s not like we need to do x amount; it’s actually about making things habitual.
So daily is, you know, five to six days a week is actually really critical, so daily contributions in terms of the diet as well as activity are really critical for that.
So I think for me, I would not actually get too stuck on that because again, there are many contributors toward that, and then what we would just try to aim at for you as a person possibly in that situation is how we amp up the other ones.
Brilliant! Everything matters, as we say.
Andrew, I’ll come to you for a clinical perspective on diet and weight and arthritis.
Cool things?
Andrew: I think just kind of adding to the history building on what Tasha was saying there, and there is some work that demonstrates that going through the process of trying to lose weight is probably as equally good.
You know, there’s not losing weight, so if you get more optical, changing your diets—particularly working with patients and talking about weight loss and the strategies to address that.
I do have, you know, because it can be obviously demotivating. You put a lot of effort into changing your diet and increasing activity, starting exercise, and then not seeing the scales move, but I think it’s important to have a home.
But the effort that goes into the process—that goes into that—is really key, really important and also can have the benefits linked to that.
I just kind of reflected on the question posed about hand arthritis; trying to draw a few things together. I should talk about the systemic information—and losing weight isn’t just about the lower loop.
There’s evidence that shows that you will reduce pain, and you reduce disability associated with hand arthritis if you lose weight, and we’ll go through that process of trying to lose weight.
Now we’re not walking on our hands, so there’s got to be something else that’s going on there beyond that mechanical load, and can sometimes be a nice way to conceptualize what it is we’re trying to think about in terms of information.
But the third thing I want to just pick up on was one of the questions from the chat about, “I don’t want to go swimming; what exercise should I do?”
To really find against that specifics, and I think we’re really bad again as health professionals of recommending swimming, cycling as the kind of default.
Really, the evidence suggests it doesn’t really matter what type of exercise you do as long as you do exercise or activity.
So my advice is if you don’t mind swimming, don’t swim. If you like walking, go for a walk. Do something you enjoy because that’s more likely you’re going to stick to it; it’s more likely to become habitual, and you’re likely to see the benefits.
There’s an NHS initiative—there’s Active 10—which is brilliant, and it demonstrates if you have 10 minutes of activity per day, you’ll start to see health benefits.
So when we think about exercise, we think about activity. It can appear daunting, but something that’s a little bit to doing something you enjoy will result in seeing the benefits. So there’s quite a bit of research into more active lifestyle approaches, etc.
Felicity: Excellent! Thanks very much, Andrew. We have, in this little bit of time left, I think, let’s talk about surgeries and medication.
I’ll come to you, Olivia, firstly, and then let’s also get your point of view, Celia, particularly about surgery.
So, Olivia, there was a question: Is there a place here for pain medication, and is it possible that we could start to reduce that pain medication by implementing some of the strategies that Tasha talked about? What are your thoughts on pain medications for the people that you’re seeing with osteoarthritis?
Olivia: First of all, with pain medication, we want to reduce the use of pain medication in any way because I don’t think anyone wants to be taking a load of tablets a day or anything like that.
So I think it's really important that we’re doing the most—the lowest effective dose for the shortest amount of time—and that’s really one of our goals in physio, especially, and through all the team that you’re working with about osteoarthritis.
To try and load you off that and get you to a point where you can comfortably manage it without pain medication.
There is a place for pain medication; we want you to not be in oodles of pain whilst you’re doing exercises and stuff like going for a walk in your daily activities.
But I think what’s good to remember is it isn’t just kind of your tablet form of medication. There are topical treatments that you can use for your joints as well, where you’re applying the creams and gels to them to try and make it a bit more comfortable while you’re doing your exercise and while you’re in that initial first painful bit of starting up physical activity.
But I think it’s really important to remember that it shouldn’t be kind of a long-term use; it should be what works for you whilst you need it.
I think that’s fine, like you’re kind of changing things, and hopefully as you change them, the need for the pain medications will come down.
Felicity: Excellent! I’ll come to you, Celia, about your experiences with both pain relief and then also the process and the decisions that you made leading up to deciding to go for surgery.
Celia: Right! When I was first, when I had—it was a telephone conversation with the GP during lockdown, and she said I wanted to get you some medication.
So I went on Naproxen, and then I was sort of having to decide myself how much I took. The pain was bad; I couldn’t walk across the street without feeling I was going to be doing some damage to myself.
So I took more, and I thought, “Well, this should help my pain, and then it will help my walking,” which in some ways—I suppose it did.
But I came to a point where I felt really quite dozy and dopey all day, so I had to think about that. It was only really once I got talking to my physio about how I was feeling that we thought that maybe I needed to think about how much I was taking.
Over time, I discussed this with my GP, and we then had a pharmacist join the GP practice, which was really helpful.
We had a good relationship there, so gradually I reduced my dose because I was out walking and more active, I was feeling better and didn’t need to have that pain relief.
One of the things that actually highlighted it for me was I got involved in some research about CI as well, and when I was doing some of the exercises, I realized I was very slow in my responses to some of the activities that I had to do in these questionnaires.
That kind of also made me stop and think. I also had to confess, with my physio listening, that I hadn’t been doing as much exercise as I should have been doing. But he was always encouraging, and he has been throughout my condition.
And it’s not always been—I’ve not always been going to see him; sometimes it’s just been that I carry on with the exercises and can contact him if I needed the support.
But that support, I think, was very important, and it was such a different approach—it was such a holistic approach.
I think what I love about the flipping pain website is that everything matters, and Tasha shared that with us today.
It was sort of in each session, we would sort of develop how I took things forward, and we would look at my progress.
Sometimes I would have to confess, and he would notice from sort of testing my mobility that maybe I hadn’t been doing as much exercise as I should have been doing.
But he was always encouraging, and he has been throughout my condition, and it’s not always been—I’ve not always been going to see him; sometimes it’s just been that I carry on with the exercises and can contact him if I needed the support.
But that support, I think, was very important, and it was such a different approach—it was such a holistic approach.
I think, I think what I love about the flipping pain website is that everything matters, and Tasha shared that with us today.
So I was also sharing that I’ve actually had surgery, and it was only seven weeks ago today that I had it.
Of course, they take scans and do things, so I know that my right hip doesn’t look great at all, but that right hip is still strong, and my plan is to keep it strong and going forward.
It may not look good in the scan, but it’s worked for the last three and a half years with me, so I don’t see why it can’t carry on for a bit longer.
Felicity: Absolutely! Brilliant! Thank you very much for sharing that, Celia. I’ll come back to talk about the surgery in a sec.
But first of all, we’ll have some questions about the pain science.
So, let’s dive into that. Tasha, probably a good one to come to here.
So, somebody’s asking that sensitization of the nervous system that you mentioned—that is something that happens over time; can it be reversed?
And there’s a question recently coming about tolerance of pain. Does that change? Does our tolerance of pain get worse or get better?
Let’s talk about the kind of the role within the threat and the nervous system’s perception of that.
I’ll let you go ahead with that first question, which was does that happen over time, that change?
Tasha: It’s quite interesting because even if we experience an acute pain experience—let’s say we roll our ankle—sensitization of your nervous system occurs right away.
When you have that tissue injury, there are rip chemicals that go out that make your ankle itself way more sensitive. But, not only that, the messages that go up to your spinal cord right away make everything in the spinal cord, and the brain, make it more sensitive, as well.
So even with an acute injury, it can happen really quickly.
What we think occurs in osteoarthritis is an interesting phenomenon because we think that the pain can persist over time, especially if there are danger messages that are coming from those joint problems, especially when you have higher levels of inflammation, where everything is much more sensitive.
So what that means is that as long as there’s still stimuli going in, it can maintain it.
In particular, if you have higher levels of inflammation paired with feeling really nervous, stress-induced, scared, all of these different things that can come in to activate pathways that go from your brain to your spinal cord for the accelerators of your system.
So that can develop quickly due to inflammation, particularly outcomes.
But the good news is, though, is that it can change.
So the graphs I showed are starting to show how slow and sure increases in activity levels over time can reduce sensitivity in the same way.
What we see with lab tests is that we can also use functional activities, like one of the things we look at is a six-minute walking test or something like that, to measure how far you can walk—so we’re not necessarily interested in how far; we really care more about how much pain ramps up when you do.
We can see reductions in how much pain or how quickly it ramps up when you're doing activity stimulus to the joint.
So we are in situational pain.
And that’s the good news—is that all the lifestyle changes in there are changeable—I would say painting in both areas—not just one.
Felicity: Excellent! Thank you very much.
I’ll stick with you, Tasha, because there are a couple of questions about other things we can change.
What can be changed, first of all?—deformities when you’ve reached a point of your arthritis where the bones have changed and you can see—the person’s case is in the hands and the feet. Can that be reversed?
Tasha: Isn’t that a really good question?
In terms of hands, the truth is I’m not sure about that.
Interestingly, there’s a lot of less research on hand osteoarthritis. I realize