– [Voiceover] I thought about drawing two different joints to show us the difference between rheumatoid and osteoarthritis. But then I thought showing it on the same picture might be easier to see the differences. But on this side we’ll keep it rheumatoid arthritis, and the other side, green, will be osteoarthritis. Let’s start with the pathophysiology of osteoarthritis which is overuse. This is where elderly people, or people who are carrying a lot of extra weight, or have extra wear and tear on their joints tend to get osteoarthritis. And first thing’s first, we have our joint space here, this is a synovial joint, so it moves. These two bones move against each other. These are gonna be the bone parts. We’re not gonna do very much with them, we care about where they come together.
This yellowish layer you see here, is cartilage. It’s kind of a cushion between the two bones. We don’t want the two bones to rub against each other. This soft, waxy cartilage, do rub against each other. Now over here we have the synovium, which is a very thin layer of tissue. And its job is to produce synovial fluid, which is a lubricant of the whole system. Synovium if you look at the word, just as an extra trivia, syn means “similar to”, and ovium is referring to the word “ovum” or “egg”.
So synovial fluid secreted by the synovium, is this whitish material, very, kind of like the consistency of egg whites. I think that’s where the word came from. Synovium, like egg whites. And that’s all filled in their joint space here, to lubricate the movements between the two bones. So as you can imagine, this system allows the bones to move every which way, gives us movement. Osteoarthritis if I had to summarize it in two words, I would say it is cartilage destruction. It is purely mechanical wear and tear of the cartilage layer, this cushioning. So we think of elderly people having this problem, but the truth is, the state of one’s cartilage is also genetic, some people have better or more cartilage to begin with. So the age issue aside, just think of it as the destruction of cartilage layer with time. I’m gonna use this bottom piece of bone to draw it out.
So this nice waxy cartilage we have will start to get destroyed. Just with time, the mechanical force of rubbing against the other pieces day after day. So some of these little pieces of cartilage might actually break off and be floating in the joint space. This is supposed to be a very pure, sterile environment, so this is irritating to have these pieces floating around. We call them “joint mice”. All it means is just little pieces, joint mice. And then if you can imagine this cartilage layer getting thinner on both sides, what’s gonna happen is the bone will get closer to rubbing against each other, and when we actually get to the point of bone rubbing against bone, we have this polishing of the bone surface. And the bones are not supposed to rub against each other, so being polished is not a good thing.
I’m gonna write “bone surface polished”. And this is where we get the grinding sound, the crepitus, that comes with osteoarthritis. Instead of sliding against each other without noise, like the cartilage is able to do, bone makes this crunchy sound. As a result of all this irritation, the bone actually starts to get these things called osteophytes. They’re like jagged edges that grow into the joint space from the surface of the bone. It’s made of calcium, and it is from the irritation and deposition of calcium. So these jagged edges are called osteophytes. This is what we sometimes refer to as bone spurs. They’re very uncomfortable and painful. They can lead to the enlargement or the change of shape of the joint. Actually there are two specific names for osteophytes in two different places. One we call it Bouchard’s nodes. Bouchard’s nodes. And these are gonna be in the fingers, but specifically in the P-I-P joint, the proximal interphalangeal joint.
So proximal means closer to the center of the body, so this is gonna be the second-to-last knuckle on the fingers. And then the other ones are called heberdenes. Heberden nodes, or heberden’s nodes. I’m not gonna write nodes there, it’s the same thing, Heberden’s nodes. And these are gonna be in the distal interphalangeal joints. Which are gonna be the last knuckle closest to the fingertips. The difference between them is the location, but it’s basically the same principle. So between the joint mice, the osteophytes, the bones crunching against each other, that’s where the pain and irritation comes from of osteoarthritis.
With rest it can get better, but it’s not gonna reverse this process. Resting allows us to slow down the further destruction. But these osteophytes are not gonna regress on its own. So now let’s come over to the other side. Rheumatoid arthritis, I like using red because rheumatoid arthritis reminds me of a whole, systemic state of inflammation, which is exactly what it is. It’s an autoimmune disorder, which means our own immune system is turning on our body, and attacking it. One thing that we associate with rheumatoid arthritis is something called HLA-DR4. This is especially important for test-prep.
When you see it, it should be like a reflex, think of rheumatoid arthritis. And this is a surface receptor on a cell that can activate our immune system to attack. In the subsequent attack that happens, if I had to summarize RA in one word, it would be “synovitis”. Remember, “itis” always refers to inflammation. So synovium is the victim of these attacks, and synovitis is what happens, inflammation of the synovium.
The synovial lining here becomes irritated and inflamed. I’m drawing on both sides, red for inflammation, that looks pretty inflamed. And as the body’s response to this inflammation, something that forms in, when we’re talking arthritis that’s very, also like a reflex you should recognize it, is called a pannus. And a pannus is basically a group, or a conglomeration of granulation tissue. I’m gonna use a different color for this. I’m gonna use brown to draw the pannus, and this is something just, granulation tissue that forms. This is just a basic principle of the body’s way of dealing with inflammation. Granulation, let me write that down here. Granulation. And granulation is kind of alive in a way, there are blood vessels and living tissue in there. And something that happens when you have granulation deposition is that it contracts. So that the shape actually changes, so contraction is again at the heart of what happens in rheumatoid arthritis. So this nice space here created by the joint capsule, because of the granulation tissue after it lays there, it contracts over time. So two things happen here with this contraction.
Number one is gonna be fusion. Literally fusing together of the bones. So when people with RA wake up in the morning, that’s why it’s worse in the morning, because you literally can’t bend. Or a more medical word would probably be ankylosing. It means the same thing, just a fancier way of saying it. Ankylosing of the joints. Number two, there’s gonna be some pulling of the joints, because the contraction is not gonna be exactly symmetrical. So because everything’s connected, when this granulation tissue pulls, the joint, the bone might shift to be over here. And this pulling dragging of the joint space leads to deformities. Kind of a crookedness to the shape, or the angle of the joints. And the stereotype is that this deformity is the most prominent in the PIP joints. The proximal interphalangeal joints. Interestingly, remember that RA spares the DIP. So the last knuckle to the fingertip usually is not affected. But the next one up, the PIP usually is. So as you can see, RA and OA kind of come from completely different directions.
And they affect very different parts of the joint. Oh, one thing I also wanted to mention with RA, we talked about rheumatoid factor. This is something you can test for in the blood that points you toward a rheumatoid disease, rheumatoid factor. And I just wanted to mention that this is an IgM, which is a class of antibodies. It’s an IgM antibody that is responsible for this, and it can tell you how severe the disease is by how much rheumatoid factor is in the body. And as a result of all this inflammation, a response to inflammation, if we took a sample of the synovial fluid, it’s gonna be high in neutrophils. Immune cell neutrophils. It’s a white blood cell, and it’s something the body recruits to the area to cause the inflammation. Without going into way too much immunology, I just wanted to include the rheumatoid factor antibody as being a key player here. It recruits the immune system to the area, and is responsible for the autoimmune reaction that happens there.
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