So, yeah, so I think what we need in order to really fully evaluate the images, we need a very systematic approach. And usually when I look at the images, I always start looking at the location of the findings, and that really helps you with your differential diagnosis. And then I look systematically at the radiographic findings. And finally, we also want to look at the pertinent MR findings, which you need to include in your report. So this is the most frequent image we see in arthritis. This is a hand image. And you always check the DIP, the distal interphalangeal joints, and the proximal interphalangeal joints first. And what you see there is mostly osteoarthritis, but you also can see erosive OA, and psoriasis is also typically found at the DIP and BIP joints. Here you can nicely appreciate osteoarthritis with subcontral sclerosis, osteophytes, full picture, that's easy. Now erosive OA is a little more complicated because the bone is quite irregular. There are little tiny microfractures, which make the joint surface very irregular, looks a little bit like erosions, unreal erosions, but you also see osteophytes and soft tissue swelling. Now in psoriasis, however, the findings are more advanced. You see more destructive change, more aggressive usually, and you also see bony proliferations. You see these bony proliferations, they are typically not found with erosive OA. And the soft tissues are also different. So as we move on, oh, this is an important finding, which you should not confuse with osteoarthritis. You see that the digit, the fifth digit, is a little curved. And you see what looks like a little bit of joint space narrowing, some deformities, actually clinodactyly, which is found in 3% of the normal population. It may be associated, however, with syndromes, for example, Down syndrome. So please keep that in mind. It's not an infrequent finding, and you should correctly classify it. So as we move on to the MCP joints, you see mostly inflammatory changes, or CPPD. Hemochromatosis is typically seen here, but what is not so well known is that osteoarthritis is a typical finding in patients who do severe manual labor. So let's have a look at this. So here you have a patient that has rheumatoid arthritis with these typical marginal erosions, very classical. That's where there's no cartilage coverage. That's where the panel's tissue invades the bone. And this is a very typical case of hemochromatosis. You have the whole picture of hemochromatosis. You have these calcifications very nicely outlined here, very nicely outlined here. You have these hook osteophytes, and you have also small subcontral cystic changes. So this is the full picture of hemochromatosis, very typical. Very frequently, however, you also see just degenerative changes on sometimes also hook osteophytes, sometimes big osteophytes, sometimes subcontrol changes. And in these patients, you should always make sure you know the history. This has been described in 1987 as the Missouri metacarpal syndrome, specifically in farmers, laborers, truck drivers. So this is not hemochromatosis. This is not CPPD. This is just bad degenerative disease in patients who perform severe manual labor. And here you really need some history on that patient. Okay, moving on to the carpal bones. Here, again, we see a lot of inflammatory changes, but also CPPD and osteoarthritis. So let's have a closer look at some findings. This is, of course, very typical. Here you have your full-blown picture of active inflammatory arthritis with these erosions at the styloid process of the ulna, which is very typical. You have these really bad erosions at the scaphoid, very, very typical. So a lot of bone missing here, very extensive also in the lunate. Now in the middle, you have a patient that has clearly CPPD. You see that the triangular fibrocartilage complex is very, very calcified. The hyaline cartilage is also calcified. And you can also appreciate this joint space narrowing, and that overall, the proximal carpal roll looks a little bit like it has lost height. So in addition to what you have here, just degenerative disease, you also have scapholunate advanced collapse, which is typically associated with CPPD. So that's an important finding you should note and you should also mention in your report. And it's also what's really important, as well, is that you should look carefully also at the hands and feet in patients with seronegative spondylarthropathies, because occasionally they also have erosive changes. And this is a very nice case where you see these nice erosive changes along the insertion of the radioscapholunate ligament. Somehow the pannus tissue, this inflammatory tissue, loves that area. It sort of grows at that ligament and destroys the bone. It's also called the test tube ligament, but it's really a radioscapholunate ligament. And these ligaments are very typically found here, not only in seronegative spondylarthropathies, but also in rheumatoid arthritis. And you have that erosion located in the scaphoid. All right, as we move on to the feet and to the interphalangeal joint one, keep in mind this is usually a joint which is not affected by degenerative disorders. It's mostly rheumatoid seronegative spondylarthropathies, and in particular, reactive arthritis. Let's have a look at some images. Here a patient with reactive arthritis. You see these erosive changes, very extensive. Some secondary degenerative disease with these osteophytes, but the joint surface overall really irregular. This is clearly inflammatory. This is beyond just degenerative disease. And here, shown on the right, very active inflammatory disease, aggressively eroding the bone, this interphalangeal joint one. So really advanced disease, very active, very aggressive in this patient with psoriasis arthritis. Now the MTP1 joint is a joint which is not so frequently affected by inflammatory changes. More frequently, really, by osteoarthritis and by gout. And even you see an overlap between gout and osteoarthritis as shown in this image here where you have this big intra-osteous tophus here, but you also have these really bad degenerative changes which are sort of happening at the same time because cartilage gets destroyed, and then you have these tophi. On the right side, you also have soft tissue abnormalities, soft tissue tophi, bad degenerative changes, erosive changes. Erosive changes are shown here, which are extensive. And then nice also shown at the TMT1 joint are these overhanging edges right here. So that's a beautiful case of an overhanging edge, again, with some soft tissue abnormality and also soft tissue abnormality at the IP1 joint. Moving on to the MTP joints to the 5-2, that's where we find inflammatory arthropathies. That's where rheumatoid arthritis typically starts. They have these marginal erosions, really nicely, beautifully shown here. So the peroneus tissue invades the bone where it's not covered by cartilage and then destroys the bone, and it looks like an apple core, as you can see here. And then much more subtle findings shown at the MTP5 joints on the right side with, again, marginal erosions and erosions also of the head of the 5th metatarsal. And one thing always to keep in mind as we move on now to the TMT joints is that in this area we don't really have typical degenerative changes and inflammatory arthropathy, but we have neurotonic osteoarthropathy. We do have, in patients that have fractures of the calcaneus and have altered biomechanics, we also find post-traumatic OA here, something important to keep in mind, but very typical is really neurotonic osteoarthropathy, where you see these really extensive subluxations of the TMT1 joint and of the entire TMT2 through 5. You see this destruction here of the tarsal bones, and really also on that CT that there's fractures, there's debris, there's sclerosis. So the whole bone TMT joints are really breaking down and including also the tarsal bones. All right, so let's now try to find a very systematic approach to looking at inflammatory arthropathies in plain films. So first of all, look very carefully. Is this now symmetric or is it asymmetric? And if it's symmetric, it's more likely rheumatoid arthritis, asymmetric, more typical seronegatives modular arthropathies. And then the soft tissue abnormalities are important, because if you look at this, this patient with early rheumatoid arthritis has really soft tissue swelling around the PIP joint, fusiform around the joint, while in this patient with psoriasis arthritis, you have these soft tissue abnormalities, which really extend through the whole finger, and this is this typical sausage digit. So this is clearly different between rheumatoid and psoriasis arthritis. Another really important finding, and this is, remember that, that's the SAM question, periarticular osteopenia is really typical with rheumatoid arthritis. This increased vascularity, which basically takes out the mineral out of the bone, and you have this really extensive osteopenia around the joint because of this significant synovitis, you don't see this so much in seronegatives modular arthropathies. They don't typically have as much juxta-articular osteopenia. So that's quite different and something to keep in mind as you look at the images. And then we have uniform joint space narrowing, which is typical for inflammatory arthropathy, and the reason is really that you see that this is the normal cartilage, and on top of this normal cartilage is the pannus tissue really eroding and chewing away at the cartilage, destroying it, and eventually leading to joint space narrowing before you see erosive changes. It is also important that you look very carefully at the subcontral lines. Now when you look, hopefully I can show this, if you look at the subcontral lines here, you see it's very intact, you see it very nicely lined up, but as you look at this, at the MTP5 joint, we have a little bit of a different situation. So you can follow it, follow it, but then you lose it. So these are really the earliest findings of erosive changes of the bone, that the subcontral lamella is lost, and then you see these really, really early erosive changes. Here you see more advanced changes, here you see marginal erosions, but these are really the earliest findings. One important thing is that in seronegative spondylarthropathies it looks a little different, and you don't really have these extensive osteopenia, there's basically no osteopenia, and then you also have these proliferative changes, which are quite extensive, and it looks a little bit like a fluffy dog. And this is really your proliferative changes, looking like a fluffy dog, and having another fluffy dog here, see these findings here at the DIP joint. So this is how these proliferative changes look like, and that's so important to correctly identify them. All right, so fine, this is the final stage, and so now everything is fused, the joint looks really terrible, and there's secondary degenerative disease, there's now disused osteopenia, so this is really the end stage. So now let's move on, the last part of my lecture, and talk about MR findings. Now, what is really good, what do we need to see? Well we need to see the parent's tissue, we need to see the synovitis, we need to look for tenosynovitis, we have to look for bone marrow edema pattern, and osteo-destruction. This is what we really see well with MRI. And I want to also clearly state what is really helpful in a clinical setting. So the clinical significance here is that you can say something much better than with plain films about the disease activity, can say something about the prognosis, and also you can monitor therapy much more sensitive than with any other technique. And here is a patient on knee MR images, contrast enhanced, which are really the best to show synovitis. And you see how this really active parent's tissue enhances very, very significantly, and it really sits on top of the cartilage, chewing along at the cartilage, destroying the cartilage, very extensive. So it really destroys eventually the joint. And there's also some bone marrow edema pattern which you can see here, bone marrow edema pattern which you can see at the femur and at the tibia. Tenosynovitis is a very important finding also in rheumatoid arthritis because it may come very early, and it is important to describe it and to correctly classify it. This is a typical finding in rheumatoid arthritis. Sometimes before you see bony erosions, because before you see anything else, you see this tenosynovitis. So it's important to mention it in your report. This has also been shown to be associated with progression of inflammation. I'm not going to bore you with classifications here, but the OMERACT has come up with this rheumatoid arthritis MRI scoring system, the so-called RUMRISC score. And it's not really important to remember it or to know how to use it, but it's important that in your MR report you include every single finding listed in this RUMRISC score, and that includes bone erosion, joint space narrowing, bone marrow edema pattern, synovitis, and tenosynovitis. All these findings need to be included in your report. And as you look at your MR images, clearly you see different things with different sequences. Beautifully shown, these erosions in the T1-weighted images, in these contrast-enhanced images, you see this panostissue, which enhances nicely. And the bone marrow edema pattern is nicely shown in these T2-weighted sequences, but also in these contrast-enhanced sequences. And this is really very important to remember, that according to the literature, the bone marrow edema pattern is really one of the most important findings if you want to assess the prognosis of rheumatoid arthritis. If you have bone marrow edema pattern, which is so extensive like this shown here, this clearly tells you, okay, this patient doesn't have a good prognosis. This is going to progress. This is really bad inflammatory disease with a bad prognosis. So let's summarize. So what we've done over the last 15 minutes is I've provided you with a systematic approach to arthritis. So first of all, we have to look at the location. Location, location, location is really important for the differential diagnosis. And then it's very critical to really systematically review the findings. Okay, first look at the soft tissue findings. Look at the joint space narrowing. Look at the bony findings, proliferation versus erosion, osteopenia versus no osteopenia. And be aware that we need to know all these key MR findings that are listed here. They need to be in your report. But you have to specifically include synovitis and bone marrow edema pattern because it's really important for the prognosis. So thanks so much for your attention. Okay, so I want to talk about six different MRI inflammatory arthritis mimics, specifically in the SI joints. I thought I'd focus on one joint. And I'm going to show them all first. And I want you to think about which one it might be, but more importantly, why and what features might help you distinguish between inflammatory arthritis and one of these entities. I'll give you a few seconds on each. Second one. Third. Okay, and before I start, I just have a confession that the request for the SAMS questions came really early and at that time I hadn't prepared my talk yet. So this is the answer to the SAMS question and if this is what you came for, you can go back to sleep now. So, okay, all right, so the first case is a 30-year-old female and the question was for inflammatory sacroiliitis and here we can see that there's a little bit of subchondal marrow edema sort of at the two ends of the joint. So what is pro for this person having an inflammatory sacroiliitis? It's bilateral, it's pretty symmetric and it's a young person. However, all of the findings are within one centimeters of the proximal and distal margins of the sacroiliac joints. And so this is actually due to mechanical stress. She actually did have a baby a few months ago and interestingly, I read that 30% of patients with mechanical back pain have some element related to the SI joints. I thought that was very high, but maybe they have SI joint pain and something else. Definitely something that requires a good clinical exam to distinguish. But also interestingly, if you're over the age of 50, 68% of you actually have some of these findings but are completely asymptomatic. So this is a case, again, you really have to correlate with the clinical history to figure out, but one thing that can be helpful is that if all the findings are within one centimeter of either end of the joint, it's less specific for inflammatory arthritis. So again, subchondral edema is only within one centimeter of the proximal and distal margins of the SI joint than really consider mechanical stress. All right, here's our next case. It's a 73-year-old female with pelvic pain. So at this point, I just wanna review quickly just SI joint function and anatomy. So the SI joints, it transmits the force from your lower extremities, the appendicular skeleton, into the axial skeleton, and it has to absorb impact from all different directions, right? Coming from below and all different angles. If you're just standing, it's already an angle from the legs into the pelvis and then up into the spine, but now add on jumping and jumping while hitting and twisting and falling and all that. And there's just impact from all different sides. And when you have something that you wanna have stability, it actually helps to have a little bit of motion too, right, if you think about like a spring being able to absorb impact. It's because there's a little bit of motion able to absorb impact from different sides. So also now about anatomy. So there's two, in order to have that stability and mobility, you have two portions of the joint. You have a synovial portion and a ligamentous portion. And the synovial portion is really the only part that can be inflamed, or the primary, I shouldn't say the only, it's the primary part that's inflamed. And it's helpful to think about the synovial portion of the joint as being anterior and the ligamentous portion as being posterior. And of course, this is a very oversimplified way of thinking about it because there are strong anterior ligaments stabilizing the sacroiliac joint, and also because the ratio of that synovial to ligamentous portions of the joint changes as you go from caudal to cranial. So here we're looking at the SI joint. The image on the left is the sagittal view just to kind of give you a reference. We're at the level of approximately S3 here at the bottom of the SI joint. If you look here, it's almost 100% synovial at this point. And as you move cranial towards S1, more and more of the joint becomes ligamentous with only a small portion of the joint being synovial. And here at the very top, just a very small portion synovial. And it's almost all ligamentous. So going back to our case, we're here pretty high up at the level of S1 and S2. And only that anterior portion again is synovial. But we see, and the posterior portion is ligamentous. And we see an extra articulation here and some inflammatory changes around that articulation. And this is an accessory SI joint, which is actually observed in up to 20% of the population. It occurs in the posterior superior aspect of the sacroiliac joint. And it can be unilateral or bilateral. But remember, just because it exists in 20% of the population doesn't mean that it's symptomatic in all of them. It just means that it's something that you'd actually notice incidentally. So if you start looking for it now, you might notice it pretty often. Here's another, just an example. This was looking for a sacral incisor region fracture, but also incidentally, she has this accessory sacroiliac joint. I just thought it illustrated it nicely. Another sort of related entity is transitional anatomy, also present in about 20% of the population. And of those with transitional anatomy at the lumbosacral junction, about 50% of those with those broad transverse processes have a pseudoarthrosis. But again, an unknown percentage have pain. But I just mentioned them together because it's in a similar location and also something that can be confused for an inflammatory arthropathy. All right, so the findings are at the cranial and the posterior portions of the sacroiliac joint, which should be ligamentous. Consider an accessory sacroiliac joint and also check an AP radiograph or coronal images for transitional anatomy with pseudoarthrosis. All right, next case is a 29-year-old female with acute right sacroiliac joint pain. When we think of this particular entity, we usually think of effusion as sort of the predominant abnormality. But actually, muscle edema, muscle edema is actually an 85% accuracy as a sole predictor for infectious versus spondylothetic sacroiliitis. And this is a septic arthritis. Here's another example. On the left, actually, there's not much of an effusion, but there is that extensive muscle edema. It's another patient with septic arthritis of the sacroiliac joint. So if there is pronounced muscle edema and the findings are only on one side, then consider septic arthritis high on the differential diagnosis. All right, next case. We have a 66-year-old female with acute right sacral pain. So this is a contrast-enhanced image. And we do see something that's potentially involving both sides of the joint. But what's unusual is that's involving the sacrum more than the ilium. So in inflammatory axiosmonoarthropathies, it involves the ilium side more because the cartilage tends to be thinner on that side. And also, the merostigminality is extending really deep into the sacrum, right? I mean, it's past the neuroforamina. So at this point, those of you who know my colleague Miriam, she would be clamoring for a T1. Oh, and sorry, and there's no definite erosions here, and maybe something actually in the SI joint as well. And here, really, the non-fat suppressed T1 is really helpful in this situation. So we can see that it's marrow replacement. And actually, also, on the ilium side, the findings there, there is some marrow replacement, but some of this signal that we see on the post-contrast images is probably reactive. And there is potentially something extending into the sacroiliac joint. So it's starting on the ilium side and go, sorry, on the sacral side and extending across the joint to the ilium side. So this is actually metastatic melanoma. And now, why does the patient have acute sacral pain? There's probably a fracture here. So she fractured, she has a pathologic fracture acutely causing her pain. Here's another related case of metastatic prostate cancer. And I think here, you can see that the axial images really help to see the joint involvement and marrow replacement, because you can compare to the other side and see the tumor, this round thing crossing and obliterating the joint. All right, so if the findings around the joint are really asymmetric, particularly if they're favoring the sacrum rather than the ilium, always check that non-fat-suppressed T1 and consider a tumor. All right, so for this case, I didn't give you the history, but now that I tell you that it's a seven-year-old male who had a chordoma that's been irradiated, I think this entity comes higher onto your list. And again, the non-fat-suppressed T1 is really helpful, and we see these geographic areas of low signal intensity on T1 and T2, and this is AVN status post-radiation. So it actually occurs in 18% of pelvic malignancies after radiation therapy, and there is a dose dependence. So the more times and the higher the dose, then yes, you're more likely to get AVN. However, no dose is safe because it's also been reported in very, very low doses. So if your patient has had any history of radiation therapy, you should definitely consider it. And the other thing is that it typically occurs more than one year after the radiation therapy. So don't consider it as something, if they died of radiation therapy within the last six months, unlikely. It's been more than a year, then you should put it higher on the list. All right, so then in this age group, it's tough to determine, is this the pain due to the AVN? Because AVN itself can cause pain, especially in the acute setting, and there is quite a bit of marrow edema related to the avascular necrosis here. And again, mechanical stress and degenerative change coexists with AVN in this age group. And so in this situation, perhaps doing an injection could be helpful to distinguish between the two in terms of what is actually causing the patient's pain. All right, so checking the T1 and all sequences for geographic areas of low signal intensity and consider avascular necrosis, especially in the right clinical history. All right, so our last series of cases, this is a 73-year-old male with urinary incontinence. And maybe there's something going on bilaterally, but if you kind of zoom out your eyes and really consider the forest rather than the trees, you can see there's actually this snowstorm appearance that goes over the entire anterior half of the image. And this is an MRI artifact, which is breathing motion, just the patient's bowel, all these little, it's just the bowel moving back and forth. And so here's another patient, a 64-year-old female with a question of seronegative spondyloarthropathy. And you can see the entire upper right corner of the image is increased in signal. Non-fat suppressed sequence again helps. You can see that the sacroiliac joint is completely normal and this is just incomplete fat suppression. All right, so if something doesn't quite feel right, always just kind of zoom out. I always lean back in my chair and take a look at the image overall and consider an MRI artifact. All right, so what do we have in our toolbox with all these cases? So as Thomas said, consider location, location, location. So in the cranial-caudal dimension, if your findings are only within one centimeter of the cranial or caudal margins, it's not as specific for axial spondyloarthropathy. If you have findings also involving the middle portion, then that's more likely to be spondyloarthropathy. At the AP dimension, if you're at the higher levels of the joint S1 and S2, then remember that only the anterior portion is synovial. So that's the portion you should be focusing on looking for findings. If you see findings in the posterior and the ligamentous portion of the joint, then think about an accessory joint and maybe a transitional anatomy. All right, in the transverse dimension, remember generally, if it's asymmetric and it atypically involves the sacrum more than the ilium especially, check your T1 and then consider something that's replacing the marrow or a fracture. And then if you see parietal muscle edema, that's very specific for infection. Always take the forest view, take a step back and evaluate the whole image. It helps to sort out artifacts. And then finally, remember, as with everything at imaging, you wanna make sure you consider multiple findings, not just something, anything in isolation. For example, fat infiltration, it's a very common chronic finding in axial spondyloarthropathy, but seen in isolation, it's in 33 to 53, even half of patients of normal and asymptomatic patients. So don't use this finding or any finding really in isolation to determine your diagnosis. All right, just one last bonus case. I'm gonna give you again, these are, sorry, it's two bonus cases because it's this one entity in two different patients. So take a second just to take a look. All right, so it looks like these sacroiliac joints are widened. And I don't know, are these subchondral erosions? And it does involve the ileum side more than the sacrum side. Well, actually this is subchondral bone resorption. And these are both cases of hyperparathyroidism, which really can look similar sometimes. So you gotta have this in the back of your head and remember to consider that, looking up just lab values can be really helpful for determining that. All right, so for all the goals of all pitfalls lectures is pretty much the same. And it's one thing, which is inception. Just to put these entities in the back of your mind. So next time when you're looking at these things, maybe you'll, something will pop up in your memory and you'll remember to think of them. And that's it. Thank you so much. A little bit of overlap with Connie's talk, because as you can tell from her SAM question, I thought she was talking about peripheral arthropathy. So anyway, this gives me an opportunity to go through some of my talk a little bit faster. I'm gonna talk about spondyloarthropathy, which is a group of inflammatory conditions that can involve both the axial skeleton as well as the peripheral skeleton and includes acute anterior venitis. But I'm gonna concentrate on the axial skeleton but I'm gonna concentrate on the axial skeleton only and involvement of SI joints, the intervertebral joints, facet joints and chest wall. The demographics of this condition are extremely important because it enormously influences how you're going to interpret the findings. So most patients present with their diagnosis between the age of 20 and 50, with the peak between 20 and 40. Their average length of symptoms is nine years. So all of the findings and all of their symptoms are usually chronic. And it's a lifelong condition with no cure, so the prevalence never declines. The most important thing though from this slide is that almost everybody has been diagnosed by the age of 50. So anything you see over the age of 50, you have to be very cautious about. A few myths I'm going to go over. And the first is that this is a disease, first of all of bone, first of all of bone, beside a joint. So the first lesion is typically iliac osteitis. And if you biopsy this in a young patient, you see an inflammatory condition that is in the subchondral bone, eroding the bone, and then it erodes from there through the cartilage and into the joint. So the spondyloarthropathies, especially in the axial skeleton, start as an osteitis and then erode from bone into joint. We divide the observations that we make into active changes and structural damage changes. We don't use the word chronic because everything is chronic. The first thing we're going to look for with regard to the active lesions is bone marrow edema, which is going to appear bright on a water-sensitive sequence. So here on the stir, we see patches of bone marrow edema, and we have some loss of marrow fat signal in a corresponding location. And these are the two most fundamental sequences. You've got to have these two sequences when you're evaluating spondyloarthropathy. The other inflammatory conditions, observations that we'll make, active conditions as well as bone marrow edema, are capsulitis, which occurs in a thin band across the perimeter of the joint. Notice Connolly has pointed out that the muscles aren't involved, so it's a thin layer of inflammation. Inflammation that occurs in the joint space. This is another myth that, this is often called synovitis in the literature, and it's not synovitis. This joint space in the synovial compartment is actually full of cartilage. There's very, very little synovium in the SI joint at all. And this inflammation occurs in the absence of synovitis. If there was synovitis here, then we would see the soft tissue inflammation and contrast enhancing around the perimeter of the joint, and you frequently don't. So this is joint space inflammation where inflammation is occurring in the higher-lying cartilage in the absence of synovitis. And then, of course, you may see joint fluid as well. Outside of the SI joints, we'll often see enthesopathy, and that will occur both at tendinous insertions as well as sites of attachment of muscle, ligament, and fascia, and particularly in the posterior aspects of the ileum, and that can be bilateral or asymmetrical. I want to show you one illustrative case because it shows you the natural history of this disease and explains some of the aspects that you're going to be looking for. So this was a 22-year-old man who volunteered for a research MRI scan because his family had a history of ankylosing spondylitis, but he was asymptomatic and actually had had some X-rays at the time just to prove that as he volunteered for this research MRI scan. The STIR sequence shows you some mild bone maroedema occurring in the left side of the sacrum, and the T1 shows you a small area of sclerosis and mild erosion in this left SI joint. The right SI joint is normal. So it is very common that erosion and sclerosis and bone maroedema can occur in an early disease, and the patient has no symptoms whatsoever. Two years later, he had a follow-up research MRI scan. Again, this is for research, and the bone maroedema has gone completely and is now replaced by this marrow fat infiltration. You can see this in some normal patients, but in most normal patients, it's completely symmetrical, whereas here, the marrow fat is very asymmetrical, and that would not be normally seen in a healthy individual. So the bone maroedema has gone away to be replaced by fat. The erosion is healing, and we see some bright signal in the area of previous erosion, which we call backfill. Five years later, he comes back for another research scan. Now, at this point in time, he has been symptomatic. He has had some low back pain, but it's well-controlled with NSAIDs. So actually, at the time of the MRI scan, he's asymptomatic at the time of the scan, and now we see multiple new lesions. On the left side, the bone maroedema is now present at the bottom of the right SI joint. On the right side, we see sacroedema and iliac edema. As well as that, we see sclerosis developing in the right SI joint, as well as multiple small focal erosions. A new erosion down here on the left, multiple erosions on the right side. So although he has been asymptomatic at this time, with all of these lesions, he's still asymptomatic. He then subsequently, about six or nine months later, became floridly asymptomatic, had a rapid deterioration, and had to then start taking biologic therapy because of the severity of symptoms. But this shows you how the lesions can change from side to side and change in characteristic. Note also that the fat metaplasia that he had developed in this left side of the sacrum has actually changed. The fat is beginning to disappear. And so when you see these fat changes, they're not necessarily permanent. They may also evolve quite considerably. So I have some suggestions here. If you're looking for bone marrow edema related to psychorhiitis, expect the edema to be multifocal, to occur on multiple surfaces, to be visible on multiple slices, and that multiple other lesions will be associated with that. In very early disease, occasionally you'll see bone marrow edema on its own, but not usually. And be very cautious about lesions that are single and small and solitary and have no other associated findings. Do not expect the findings to be either bilateral or asymmetrical in this early disease because the lesions move around. They're constantly, slowly, but constantly moving from ilium to sacrum and from right to left, et cetera. So it's hardly ever symmetrical and very frequently unilateral in the early stage of disease. The structural damage changes I mentioned, we're gonna look for our sclerosis, which is very nonspecific. Fat metaplasia, erosion, backfill, and ankylosis. So the sclerosis is nonspecific, but if it's five millimeters or more in thickness and in males, it is suggestive of spondyarthritis. The fat metaplasia is also nonspecific, but when it's due to spondyarthritis, it typically has a sharp edge, borders the articular surface, and is relatively homogeneous, and it's related to the heel bone marrow edema. Erosion is the most specific single lesion and is seen even in early disease. It's very common to have small erosions even in the earliest disease. These may be seen as small focal rat bites or as diffuse areas of erosion of the articular surface. As the erosion heals, we get this pattern of backfill where you get bright signal in the erosion cavity, and this may then progress to ankylosis. Backfill, defined in 2012, is a healing phase of the erosion where we see bright signal in the erosion cavity with an obvious area of sclerosis separating it from the underlying bone. The most important thing for the SI joint is the global opinion. You may look for all of these features, but their distribution, location, and the relationships to each other are extremely important in determining your final opinion on that. Be aware of tremendous anatomical variation, and Connie showed us a few, but the SI joint is subject to the most extraordinary variations of acute angular contour, even in normal patients that can mimic disease. You can have posterior clefts where ligamentous clefts run deep into the ilium, and it has been reported sometimes that there's the appearance of a double joint, but you never see the joint twice on a cross-sectal image, whether it's coronal or sagittal. You never see the joint twice, and if you see two clefts, the medial one is always the joint, and the lateral one is always the ligamentous cleft in the ilium. This is occasionally confusing in MRI where we don't see the bone quite as well, and you can have bright areas of fat that's actually in the ligamentous cleft, or vascular structures that can look like bone marrow edema. Sudarthrosis, Connie has talked about, but we also see deep ligamentous insertions which can appear in the center of the joint, or vascular channels. So anatomical variation in the SI joint is extremely common and is expected in every case. What else could it be? I'm gonna talk a little bit about this, but I'll skip a few slides where it's not relevant after Connie's talk. If we look at bone marrow edema, obviously it's seen very frequently in angst, bond, and in patients with early disease. This is inflammatory back pain, but it's also seen in 20 to 30% of patients with mechanical back pain and perfectly normal healthy volunteers. Fat lesions may also be seen in a quarter of patients, but erosion is seen less often. A more recent publication has shown that in young athletes, and this was a group of recreational runners and elite ice hockey players, they saw a small foci of bone marrow signal change in up to 41% of their subjects. So small foci of fat signal change or bone marrow edema are very nonspecific. With regard to the normal joints and mild osteoarthritis, these lesions occur around the perimeter of the joint, anywhere around the perimeter, although they're more common, posterior inferiorly and anteriorly. But they do occur anywhere around the perimeter of the joint because the perimeter is where focal mechanical stress occurs most prominently. Here's a patient with a small focus of bone marrow edema on two consecutive axial slices, but this is a typical location for bone marrow edema due to osteoarthritis. Obviously, we see changes in osteoarthritis condensans, ILE, erosion may occur, but there should be very little erosion, very little bone marrow edema, very little fat metaplasia, but it is the condition that is most difficult to distinguish sometimes from spondyloarthritis. Changes in pregnancy can produce a solitary erosion and some inflammatory signal changes, but there's usually no fatty changes and the history is critical. An insufficiency fracture would typically affect one bone only, so there's no erosion, no fatty changes, and only one articular surface involved. And as Connie pointed out, muscle edema and septic arthritis is a critical observation that clearly distinguishes these septic patients from spondyloarthritis. You may also get spondyloarthritis in erosive arthropathy, so here's a case with CPPD, but most of the CPD patients are much older, in the ages of 60 to 90. And here's a patient with extensive erosion in an 87-year-old. There's bone marrow edema and erosion and sclerosis, and if this was a much younger patient, you might consider SBA, but this is CPPD. And also in gout. In patients with established facial gout, 35% of them have involvement of the axial skeleton, and the age range does overlap with SBA, but they usually have a known diagnosis of gout elsewhere in the body before the spine's involved. What sequences should you perform? Three semi-coronal sequences we recommend. Bone marrow edema. Any water-sensitive sequence will do. You should not use proton-density Fatsot or intermediate-weighted imaging, because the red marrow's bright on proton density, and you don't need DWI or gadolinium. It's not necessary. For erosion, use a T1-weighted Fatsat sequence. It could be either T1 or gradient echo 3D volume, and it's been shown that the really thin-slice 3D volume MR looks identical to CT, but be aware that the higher resolution you have in MR, the more you're going to see small erosions in the normal healthy population. And of course, you need a T1-weighted sping and echo to look at fat metaplasia and backfill. Note that with this combination, with needing a T1 Fatsat for erosion and a T1 for fat metaplasia and backfill, this is the ideal situation for doing a Dixon sequence, where you can get both in a single acquisition. So we're investigating that. Should we ever do CT of the SI joints? Well, occasionally, I would recommend doing low-dose CT. Here's a 41-year-old female with a small patch of bone marrow edema that might be biomechanical, but the CT shows very clearly that there are some erosions. I'm going to flip through the spine in just a couple of minutes. We're going to look for anterior spondylitis, corner inflammatory lesions at the thoracolumbar junction in particular. Very common, but they're nonspecific, and the shape and distribution's extremely important for that. Spondylitischitis may spread across the entire disc, but there's no soft tissue inflammation. And again, the soft tissue inflammation distinguishes from infectious discitis. Note that in the post-lateral corners, costovertebral disease is very specific for SBA. So you see inflammatory lesion here. It's very specific for SBA. And further out laterally, you can either have enthesopathy or ticular disease at the cost of transverse joints that is very specific for SBA. The structural damage changes in the spine due to fat follow the bone marrow edema changes. Note that these can be very vertical, and this is very specific for SBA. Some of these small lesions may be much taller than they are horizontal, and again, that's suggestive of an inflammatory cause rather than a mechanical one. How many corner lesions do you need? Here's a patient with premature senile kyphosis with multiple anterior inflammatory lesions, but she has degeneration in the spine. And so the answer is to not count them. We can see small corner fat lesions in even completely normal healthy controls, so counting them isn't helpful. If you had a 22-year-old male with perfectly normal discs and just one or two lesions, you should consider spondyloarthritis in your differential diagnosis. And there's also patterns that are important. So if you see small fat lesions in all four corners of a vertebral body, or if you see them four in a row, that's highly suggestive of SBA. So don't count them. Two lesions may be enough or not enough depending on the age, history, and degeneration. Don't worry too much about the anterior chest wall. You often see findings, but they're not very specific, and it doesn't often help to make the diagnosis. So the most important things are good clinical history, experience with the range of findings, and awareness of anatomical variation. Be aware that the SBA lesions are often multifaceted, multiple locations, multiple characteristics, multiple distribution. Those are extremely important, and the mechanical ones are small and solitary. Thank you very much. And so today I'm gonna be talking about the nuts and bolts of quantitative cartilage imaging and what it takes to add this to your clinical practice. Well, when there's macroscopic disruption of cartilage, standard morphologic imaging does a pretty good job at detecting and characterizing lesions, whether they're at the surface or if they're deep delaminations at the bone cartilage interface. But difficulties still arise with thin cartilage fissures that are subject to partial volume averaging when cartilage defects are completely filled with damaged cartilage, and especially in early disease when abnormalities are microstructural and due to loss of matrix components. Many severe cartilage injuries can be quite subtle on imaging because we don't see the cracks in the surfaces, as we can see in this case, or we don't see the separation at the bone cartilage interface. And in this case here, there actually was no communication with the surface, but as it was probed, the cartilage moved over the bone, much like a rug on a loose flooring, and you can see it's quite a large lesion there. So how should we interpret abnormal cartilage signal when it appears morphologically intact? So for instance, what is this? Is this a defect that's filled with damaged tissue, or is there lost proteoglycans from otherwise intact cartilage? And what I want to say is that compositional imaging, or parameter mapping, has proved sensitive for finding alterations in the internal microstructure and the biochemical composition of cartilage matrix, and we can hope that imaging techniques that are sensitive to cartilage matrix changes can improve our diagnostic capabilities. Cartilage tissue is largely made up of extracellular matrix composed of proteoglycans held within a highly organized collagen structure, and this extracellular matrix is produced by the embedded chondrocytes and gives cartilages properties. The proteoglycans are mainly aggrecan, which form large aggregates around a high-uranic acid core, and they are highly negatively charged because they contain many glycosaminoglycan molecules that have sulfates and carboxyl groups. This negative charge is called the fixed charge density because the proteoglycans are trapped within the tissue, and this results in a highly osmolar matrix that attracts water, and that leads to the structure that reversibly resists compression and is self-lubricating, and that's why cartilage is so good in the joints. The collagen molecules are arranged and ordered in a macrostructure, and some of the MR parameters may be affected by the orientation of the collagen, and that's what the magic angle effect, and so here in this study by Doug Goodwin, we can see the T2 values differ with the collagen orientation. So what is cartilage mapping? It is actually displaying these tissue characteristics obtained through our imaging techniques, and each of the voxel values really is related to the parameter that's calculated from the images rather than simple signal intensity, and often the map is displayed in color superimposed over morphologic image, and that's probably what you most commonly see in the literature. Typical parameters for cartilage are contrast uptake or MR parameter measurements, and then finally direct sodium imaging. So in this example that I'm showing, we have seven spin echo images, each at a different TE, and from that you can get the T2 relaxation value and then map that over by curve fitting all of the signal intensities on those seven images, and that's a typical thing that's done. So there are many choices for cartilage mapping, and I'll go through some of them just briefly. You can see that using an ionic contrast agent, you can actually get the proteoglycan content because the concentration of the contrast agent will be inversely proportional to the local fixed charge density. For CT, the changes in attenuation come from the iodinated contrast that's measured, and for MR, the T1 measurements are shortened in the presence of contrast agents, and those are mapped. For the most commonly used ones that have been studied, these are T2 star, T2, and T1 row, and these are sensitive to the macromolecular content. T2 star uses a gradient echo image, and therefore it's sensitive to field inhomogeneity. However, it's really good for rapid acquired sequences and 3D acquisitions. T2, while more robust, is sensitive to organized collagen, orientation, and magic angle effects. T1 row, depending on the strength of the spinlock pulse, is not as highly influenced to magic angle effects. However, it's not currently available commercially. Magnetization transfer techniques can also measure cartilage macromolecules, and they require at least two sequences, one with an off-resonance pulse and the other without, and then you calculate the degree of tissue saturation caused by that off-resonance pulse. And GAG-SEST, a technique being used at ultra-high field, is a magnetization transfer method that's specific for glycosaminoglycans. Diffusion imaging methods use applied gradients to calculate the movement of water within the cartilage matrix, and even diffusion tensor imaging of cartilage seems to be feasible. Finally, direct sodium imaging, since sodium is a counter ion to the proteoglycans and the negative charges, if you image this directly, you can get a map of the proteoglycan content, but because the lower signal-to-noise ratio of sodium imaging and the relatively low concentration of sodium compared to protons, ultra-high fields such as 7T is required to get good resolution. So in summary, there are many different options for mapping cartilage parameters, imaging parameters, but as shown by this ex vivo study, all of these can be complementary. So we can see here where the GAG and degenerate map is different than the T1 row, and that's different from the T2. And so what we, and so far, all of these have been really used in research studies, and so what have we learned from those research studies can help us bring these into clinical practice. First question is, can we produce reliable measurements and what's required to get them? So the Osteoarthritis Initiative ran over 13 years and it imaged over 4,500 patients' knees at four different sites. But they were really strict with this. All of the systems were identical and running the same protocol. Quality insurance checks were performed with phantoms every day of imaging prior to the patient's imaging. And we can, but we can see from this graph that over eight years, the T2 value is very less than 5.4%, and that's really quite good, and that's despite an MR upgrade. And at times, the QA phantoms were able to detect variations in different parameters that required recalibration of the magnets. Measurements, however, are sensitive to the equipment being used. And here we can see that using the different coils can result in different results. So these cartilage T2s are measured for the same subjects and on the same magnet system with the same protocol, but either with a quadrature transmit receive or a quadrature transmit phased array receive coil. You can see that T2 values were from lower SNR, quadrature coil were systematically shorter than for the higher SNR phased array coils. And so better SNR images produced higher T2 values, and when low signal echoes are added, it's actually the curve fitting that gets off, and that results in what look like shorter T2s. Therefore, an SNR of at least two for the last echo is recommended. And some of the analysis software available for manufacturers will allow you to set the level of noise where they will no longer calculate those echoes within the T2. Not surprisingly, the measurements, even though T2 is another, and T1 row should be specific for tissues, using different pulse sequences can give you different values. And here we compared T2 values for spin echo, multi-echo spin echo imaging, and 3D map sequence, and we can see that the values for the 2D spin echoes were higher than for the 3D maps program. So in summary, a whole host of things can go wrong and mess up your mapping values. And this is just a list of some of them. And this makes longitudinal and cross system reproducibility quite challenging. And that means without careful calibration checks and direct comparison of patient's MR parameter values over time, or when obtained from different systems, really may not be reliable. So that limits what you can do comparing time point to time point. In this systematic review of 58 studies that looked at test-retest reproducibilities, you can see, however, that each of the parameters, DGEMRIC, T2, and T1-Rho, had really good test-retest comparisons when you looked at the major compartments. But if you start looking at the actual value for small regions, the variations can really be quite high, and they were up to 19%. So for small regions, that can be even greater than the pathology changes you might expect. So you need to be very careful about that as well. So what can we do? It's probably the best thing is single, looking at comparisons within a joint. So the good news is that within a single study, since the parameters are the same, comparing region to region should be valid. So if you've got an area with abnormal values and normal values, you can rely on that. Likewise, on follow-up studies, you can look at changes, either improvement or progression, within a joint, and those findings should be real as well. But I think the real question here is why would I want to do this in my practice? Yeah, well, Dr. Kajowski did a study, and he found that we can improve the detection of early cartilage lesions by just adding a five-minute T2 map to the standard clinical sequences. And the question is, when would that be important? Because after all, nobody really has a treatment for early lesions like you might have for low bone mineral density. In one of the first compositional imaging reports about the hips, Youngjo Kim in Boston found that preoperative degeneric analysis of hips with developmental dysplasia could predict the surgical outcomes, and patients below a certain threshold really had a worse outcome. So that information could be used to inform patients about the odds of success and potentially avoid surgeries that are doomed to failure. And this new article coming out in the Journal of Cartilage reports about surgeons' dissatisfaction with radiologists reporting a cartilage defects. And this was preoperative MR arthrograms in patients with ephemeral acetabular impingement. We had a very poor sensitivity for acetabular delaminations. Our specificity was quite good, but what we don't know from this paper is whether this was a problem in actually seeing the lesions or whether this was a problem in radiologists not knowing that it was important to report them. But since FAI surgery is worse for patients, outcomes are worse for patients with cartilage abnormalities, it's good to know these things ahead of time. A number of groups have reported techniques for compositional imaging for the hip, including 3D methods for degeneric and T2 star, and the reports show good correlation with surgical findings, like in this study here, where we can see the abnormal degeneric index in the area of the cartilage delamination. And the group from NYU really did a nice job in terms of comparing areas within the joint. They supposed that the cartilage near the fovea would be more normal, and so they standardized their degeneric technique, degeneric values to that cartilage producing a Z value, and then used a threshold of the Z value, and they could see that using the standardized degenerate, they were able to detect and say this cartilage was abnormal, which it was at surgery, but that using just a standard threshold, it was not detected. So by this region-to-region comparison, they really removed the intersubject and interstudy variations in cartilage T1 caused by differences in contrast delivery to the joint, or natural variations between patients. Cartilage repair surgeons determine their surgical options really based on cartilage lesion size. And so the repair size for them includes any surrounding abnormal or unstable cartilage or cracked cartilage like we saw before that they have to debride. Not surprisingly, morphologic MR imaging tends to underestimate the final size of the cartilage repair as we can see in this case, where it looked like it was a really small lesion, but then when they took out all the bad cartilage, ended up much larger. So when we report these lesions, on preoperative MR, should we be reporting just the clearly damaged cartilage in here, or should we be looking at anything that has abnormal subchondral marrow changes or abnormal cartilage signal where it's a little bit brighter? And will this larger area be abnormal and need removal? And I found this case interesting. So this was a patient had this defect here and it was treated with microfracture. Nine months later, it came back with more symptoms. And the microfracture is doing fabulously, but you can see that there are new cartilage defects here and on each side of the repair. So is this progression of osteoarthritis, or did we just fail to alert the surgeon about an area of insufficient cartilage next to the defect? And could this outcome have been avoided with compositional cartilage mapping? So what can we implement now? I would say that we can do T2 star and degenerate cartilage mapping successfully with regional cartilage analysis. And the clearest indications are for surgical planning. Time management is really important, and this is probably one of the biggest problems. How do you do all of this and still run a good service? So what you can do is you can have your cartilage maps really do double duty, because you get the image, several echoes. You could substitute some of your other images that are obtained during the T2 mapping for those. And recently, there's a new paper out where they've actually calculated images from the T2 mapping sequence. Or you can do a faster routine protocol, but there you're probably gonna be sacrificing your image resolution, or you could acquire fewer images in series. And then, of course, we need to get faster cartilage parameter acquisitions. But really, the thing is, be selective and figure out which patients where it's worth spending that extra time. And also, are your surgeons gonna act on this? Post-processing images. Now, some systems have automated images, and you usually get an image like this where everything has a T2. If you wanna produce an image where you're just looking at the cartilage superimposed on another image, that's gonna involve some offline manual or semi-automated tasks. So where are we going? Right now, we do everything manually, but a lot of people now have developed machine learning programs that are doing automatic cartilage segmentation, and this is, I think, where things are gonna go so that we can have all of this routine. And we can produce these reports for referring physicians where you give a cartilage map, but this really takes time at this point. So in conclusion, implementing cartilage mapping requires attention to detail. It's useful for highlighting occult lesions, good for patient selection for surgeries and assistant planning, but these analysis need to go into standard workflow. I wanna thank everyone who helped me put this together, and thank you for your time. So moving forward, advanced CT imaging. This is a combium CT. This is a picture of the computer tomography. It's a very small device. You can put it in any orthopedic clinic, and it was initially created at Johns Hopkins. This is the first prototype. This is not a commercial one. As you can see, it's really ugly-looking. It was initially created in 2014, 2013 at Johns Hopkins by my senior BME colleague, Jeff Stewardson, and the idea was to do a weight-bearing and non-weight-bearing CT acquisition of lower and upper extremity, of course, and then also upper extremity in a non-weight-bearing, of course, mode. And the analogy was akin to a radiograph of foot and ankle or knee, weight-bearing versus non-weight-bearing. So the first thing that we did about four, three, four years ago was to look at the image quality of the combium CT and trying to compare it with the conventional MDCT that we usually take, imaging acquisition of peripheral extremities for different reasons, including osteoarthritis, and the interesting thing is that if in regard to the bone image interpretation tasks, with regard to bone, this devised it pretty well. As you can see, we have a nice, better evaluation of the trabecula, bone trabecula, compared to the MDCT, but when it comes to the soft tissue visualization task, it has a little bit less of the contrast resolution compared to the MDCT. So when we did evaluate this image quality systematically, we found that there's an excellent image quality for bone visualization tasks, but it's adequate. That's how we grade it with regards to the soft tissue visualization task. And moving forward, then we started looking at this device to see what's its potential with regards to the osteoarthritis. And one of the things that we figured out, there are some elements of injury or biomechanical derangement that you cannot fundamentally detect or you have low sensitivity to detect using non-weight-bearing imaging. A concrete example of that is a meniscal extrusion. There have been papers published in the literature that specifically say meniscal extrusion is associated with the worst osteoarthritis outcome, including knee replacement, worsening pain, and full thickness cartilage loss during follow-up. So when you do weight-bearing now, you have a capability of measuring the meniscal extrusion and compare it between the weight-bearing and non-weight-bearing acquisition. This clear example on top, you can see that the meniscal extrusion is getting worse up to three millimeter when you apply weight-bearing, physiologic weight-bearing, and these are important because they can add to what we see in anatomical imaging, non-weight-bearing MRI or CT imaging. Moving forward, the next relatively novel CT technique that I have been working on in the last seven and eight years the idea was actually coming from the cardiology and cardiac imaging. The first prototype Aquilin-1 Toshiba scanner, 320-year-old multi-detector CT with 0.5 millimeter pixel size, which equals to 16 centimeter of coverage of any body part was primarily designed to evaluate heart, freeze the heart in one acquisition, gantry rotation, and also for CT perfusion of brain. My mentor, John Carino, when he was at Johns Hopkins, when he recruited me, he said, okay, there is an opportunity to look at the peripheral joint motion because most of them can be completely imaged in this 16 centimeter size, gantry size. So we did try it. This is the temporal resolution of, this is 0.5 seconds, so if you wanna do it, you should instruct the patient, train the patient to make the motion not too slow, not too fast, so you can get an optimized image quality with regard to the peripheral joint motion. And if you look at the literature, it has been used to evaluate motion of the wrist, ankle, hip, elbow, and knee. The yellow color-coded joints are the ones that I have done primarily at Hopkins, and the font size is correlated with the number of cases I've done. Most of the cases we have done at Johns Hopkins was knee, and any, with regard to any CT technique, especially when you have a motion, a lot of image acquisition, the first question is the radiation dose. There's a lot of radiation dose, but when it comes to effective radiation exposure, because the skin is the only radiation-sensitive organ in the filibu, you will see the actual, you know, effective radiation dose is not that high at all. It's between 0.3 and 1.5 millisievert, and this is a table I adopted from Mettler's famous paper in radiology, which point out that this is not really a high radiation exposure when it comes to effective radiation dose calculation. So it's pretty safe to do it in the clinical practice. This is an example. You can see, orthopods, orthopedic surgery colleagues love this picture because they show it to the patient. They show that, you know, the patella is popping out in this patient who has, like, patella maltracking. But, you know, as a radiologist, we need to do more analysis. Just pretty image and pretty movie is not enough, I would say. So that was my motivation to look at this. This is the first real paper that we tried to publish in 2014. These are the patients who had unilateral patellar instability, and we showed that the contralateral asymptomatic patellofemoral joints in these subjects have abnormal measurements because this is a developmental thing. One side goes bad, becomes unstable, but the other side is not normal either. So we looked at a bunch of measurements, like TTTG, patellar ALTA, and all those things, and also we did some measurements during the dynamic motion, which is a patellar bisect offsets at different angles. And we figured out, okay, using the regression model, both static and dynamic measurements can indicate which asymptomatic contralateral joint has imaging feature of osteoarthritis. So this is something interesting. That tells me that not just static imaging measurements, biomarkers are important, but also there are imaging biomarkers that can be obtained using dynamic imaging. And that can have a huge new era of investigation with regard to the osteoarthritis risk stratification using advanced imaging. So moving forward, advanced MR imaging. My disclosure is that at my institution, we don't do any of these following slides. I got this slide from my senior colleagues. The first slide is just a panoramic view of the all compositional MRI sequences. My senior colleague took analysis events through the most common ones, and I don't wanna be really redundant here. The red, the yellow color-coded lines are the ones I'm gonna briefly talk about as really something new that is coming up in terms of complementary. I quote his word, complementary new sequences that can further evaluate the quality of the cartilage. The first one is sodium imaging. It is a very technically challenging technique. We don't do that at Johns Hopkins. You need fundamentally to have a seven tesla or higher strength magnet to do it, and you need a specific coil and software to be able to do the measurements. This is a concrete example of how sodium imaging can show abnormal cartilage with regard to the fact that morphological imaging is quite unremarkable. And moving forward, you can see there is another new advanced compositional MR sequence which is called GACCEST. As you can see, this is quantifying exchangeable protons, including those that you've seen a glucosominoglycan, and then you also can detect areas of cartilage abnormalities. This is an example that we got from Dr. Gary Gold from Stanford, it's the basketball player study. Pre-season and post-season, as you can see, the central femoral condyle, sodium MRI sequence, compositional sequence clearly show that there's a signal loss here that we cannot detect in other compositional, conventional compositional sequences. Let me put it this way. And moving forward, there are some other advancement in the compositional sequences rather than with the older ones. Now there are capabilities to do a 3D isotropic voxel acquisition with the technical fast imaging that is actually going to this direction as well. That helps with the feasible, accurate, repeatable, and precise determination or measurements of cartilage quality. And now we can evaluate the cartilage at multiple planes. That is good and maybe bad because if you just go to multiple plane, that may have another point of variability and lack of agreement. That's the biggest problem in this kind of quantitative assessment. So this also has to be further investigated, how much is an effect measurement and consistency of measurements using compositional MRI sequences. A few other slides to conclude OA PET imaging. FDG PET CT imaging is very common for oncological purposes. We do recommend looking at the joint in any PET CT that you guys need for different purposes because the synovial inflammation that is an integral part of the osteoarthritis can be shown and easily detectable in the PET CT examinations. And that's actually very important to put in the report and impression of report because there are reports that saying that synovitis can be treated or can be fixed or can be helped by common medications such as NSAID or corticosteroid injections. So these are some things to have in mind and this is an opportunity. I don't recommend doing a PET CT to evaluate osteoarthritis but if you have it in oncological patients, then that's something valuable to look at and to characterize. And then, you know, given the poor anatomical resolution of osteoarthritis changes with PET, researchers have used PET CT to develop special model for early detection of OA. PET has been used to combine with MRI to evaluate from hand OA and there's a sodium F18 PET CT and PET MRI to look at subchondral bone uptake. So these are a lot of activities with regard to osteoarthritis evaluation that's beyond the scope of this lecture. This is a kind of a relatively old, 10 years old study looking at the PET MRI and the fusion of PET with MRI images to look at the hand arthritis, arthritis in DIP joints. That kind of investigation dropped at some point and now this technique is mostly used for evaluation of early rheumatoid arthritis. This is a case that we put in a review about three years ago with regard to looking at the FDG uptake of synovial lining in the setting of osteoarthritis of the shoulder and knee. And as you can see, there is a circumferential uptake of the FDG and this is something worth of mentioning in the report regardless of primary reason why the patient got the PET CT which probably was a cancer follow-up. And thank you very much for your attention.

imaging techniques

arthritis diagnosis

radiographic findings

MR findings

differential diagnosis

joint evaluation

osteoarthritis

rheumatoid arthritis

advanced imaging

cartilage degeneration

PET imaging