Tuesday Nite Rheumatology (on 11.18.25) Save

This podcast is a preview of the great lectures and speakers you'll hear at RoomNow live twenty twenty six, February in Dallas, Texas. You can register at roomnow.live. In this podcast, you'll hear some of the speakers and lectures from RoomNow live '20 twenty five, specifically on RA, PSA, SPA, and vasculitis. Hope you enjoy it. Welcome to Tuesday night rheumatology.

Hi. I'm Jack Cush with RoomNow. This week on TNR, we'll be discussing spondyloarthritis. This is a replay of RoomNow live 2025, which took place back in February in Dallas, Texas. Today, we're going to replay the spondyloarthritis pod.

We wanna thank our sponsor, AbbVie, for supporting Room Now Live and for sponsoring this pod on spondyloarthritis. RheumNow Live is coming up in February in Dallas, Texas. We hope you'll be there either virtually or on-site. It's gonna be an exciting meeting. Tonight, we have excerpts from three great lectures on spondyloarthritis.

First, Desiree Vanderheide is going to talk about advances in the treatment of spondyloarthritis. Second, Jennifer Cather is going to be talking about progress in hidradenitis suppurativa. And third, Doctor. Catherine Bakewell is going to talk about imaging and evaluation of patients with spondyloarthritis. Our first speaker is Desiree Vanderheit.

She'll talk about disease modification in SPA. Desiree is professor of rheumatology at the Leiden University Medical Center in The Netherlands. Take it away, Desiree.

So can drugs inhibit radiographic progression? Well, we have the very old data from the Wando study, where there was a continuous use of NSAIDs, a certain on demand use of NSAIDs, and there's a significant inhibition by the continuous use. It's important to realize that although the use of the NSAIDs was free, most patients used silicoxib. But with further analysis of these data, we saw that patients have normal CRP, there was no influence, but only the inhibition could be seen in those patients with the elevated CRP. Then there was a later study, the MRata study, and here they used all patients use diclofenac.

And here it was again continuous versus on demand, but there was no clear effect of the continuous treatment use. So what can we conclude so far on the NSAID use? Patients with normal CRP, there's no effect of continuous NSAID use, and patients with a high CRP, we have conflicting results. We had a positive trial. There was another positive cohort study, but that did not show, and a negative trial.

So the question is, could that be due to a differential effect of NSAIDs, for example, celecoxib versus diclofenac? Then another important treatment modality are the TNF inhibitors. And as it is very difficult to do a double blind randomized controlled trial, this placebo versus TNF inhibitor, because you know very soon it will be unblinded as you know which patient has a TNF inhibitor. So, it was decided to compare that to historical control data from OASIS. So, those were radiographic data collected before we had TNF inhibitors available, and we used the early studies of the TNF inhibitors.

And you see that there was no inhibition of radiographic progression over those two years. Then you can also see this in probability plots. So again, this is ordered from the lowest progression score each individual patient to the highest progression score if you go to the right, and you see that in gulimumab trial, which was a trial that was later seen, but still in the early phases of the biologicals, we have all about the same data. About forty percent of the patients, they show progression and the mean M cells progression around 0.8, 0.9. Then we had later data, and there is, for example, the rapid XPAR trial sotilizumab and the secukinumab measure one trial on secukinumab.

And there we saw that there were fewer progressions, only twenty percent, and also the mean mSAS progression was lower. So then the question was arising and that was especially with the secukinumab data as this was a new class, is there an inhibition of structural progression by these new drugs? Well, I think there we have some difficulties, because the older trials, they have higher MSA scores and also higher CRP at baseline. When we started this Axial Spy in 2002 with the two inhibitors, we had the reservoir of very severe untreated patients waiting for trials. We could include twenty five patients in a single center in a very short period of time.

But when we were later in time, for example, the trials that were run-in 2018, there was a depletion of the worst cases. These were already treated in clinical care and it was hard to find eligible patients for studies. So, we are including completely different patients in these later trials. There's also a comparison of the measure one study with cicakinumab and diclofenac data from MRADAS, and there if you look at the probability plot, again, there is really no difference between the two groups. So then the question is, while it's so difficult to gather true answer from clinical trials, will observational studies give us the answer on treatment effect on stroke percussion in axial SpA?

We have some data from a cohort study from Switzerland, and there there were two hypotheses. First is TNF inhibitor leads to the inhibition of syndesmified progression, so that would be a direct effect, or is there an indirect effect by suppressing disease activity? And if you look at the data, then the first line is showing that indeed the TNF use prior to a radiographic interval resulted in a fifty percent reduction of radiographic progression. But if you looked at the mediation analysis, then there was no direct effect of a TNF inhibitor on progression, but only an indirect effect via Asthat. So this is important to know because we can also use that in clinical practice.

And here is our data from this study and you see that especially patients who have inactive disease, that means the is below 1.3, those are the patients with lower radiographic progression. We also have other observational data from The US, Berlin Genssel did various comparisons with a two year or a four year follow-up, so the early or the later effect it was called. And if you have patients got only TNF inhibitor monotherapy, there was no effect, not early and not late. If patients got a TNF inhibitor plus a low dose NSAID, there was a late effect, so after four years but not after two years. And if you had patients with a high dose NSAID in addition to a TNAV inhibitor, there was a late effect again.

And if you had patients with a TNAV inhibitor plus celecoxib, there was also an early effect, and of course also the later effect. So this is hinting again that there could be a differentiation between the diclofenac used in earlier studies and celecoxib used in different studies. This is the paper that you also had in your pre read material, and this is looking at observational studies, so a review of all the different observational studies, but then looking and evaluating through the lens of causal inference, and that means that you can also draw causal relationship even in observational data. And from this data, taking everything together, it could be shown that BD MADS might slow spinal structure progression, and by suppressing the inflammation, so that's also what we saw in the Swiss cohort. Then we had more recently a clinical trial comparing cicadunumab with adalimumab, so this was of major interest if we could see a difference between two different biologicals.

And what we see here is the response rates of the patients showing progression in the mSALs, and there was absolutely no difference between two different doses of secukinumab and adalimumab. And also, if you look at the MSAS progression, also there is no real difference. Sometimes you see in the MSAS progression some numerical differences, but that's usually caused by outliers. Then an even more recent trial from last year, we have the COMSOLD trial comparing colimumab versus colimumab plus silicoxib. So, we were really expecting a lot from this trial, because it's included in patients with radiographic XBA who have at least one syndesmophyte, or an elevated CRP, or both.

And then they were followed, there was a first run-in period of twelve weeks and patients who had a clinical response, then they were randomized to the colimumab monotherapy or colimumab with selecoxib. And here you don't see a difference, a significant difference between the two groups. But you also see that we have quite low patient numbers on top. Those were the patients that were randomized. On the bottom, you see the patients that completed the study.

And the left is the main change in the mSATs, and the right is the development of new syndesmophytes. So you see that in both there is a trend, and especially you see that in the development of the new syndesmophytes, but the number of patients is rather low. And that's also what you see in the probability plot. You see that there is a tendency to show a discrimination. And you also can see here in the table in the right that especially if you take out the patients who have the double risk factor, the CRP and the syndesmophyte, there you start seeing an increasing difference between the two groups, but these are very low patient numbers.

So it's a pity that this trial had only a few number of patients included, so we still do not get a definite answer as there is a tendency to show a difference, but the trial seems to be under power to have a significant difference. Then if we go back to our clinical case, we had our male patient, 38 years old, axial SpA since nine years, clearly elevated 2.9, usually high disease activity is seen as above 2.1. Also an elevated CRP, dysendezomophytes, and we concluded that he had a total of six risk factors. His treatment is diclofenac one hundred and fifty milligram daily. So what would be the next choice?

Personally, I think that this patient with so many risk factors should get a biological and then you can choose between either an IL-seventeen inhibitor or a TNF inhibitor, as we do not have differential aspects with the effect on structural rate of progression and also not on the clinical. Another debate is what to do with the diclofenac to either change it to Iturcoxib or cilacoxib or another COX-two inhibitor or just give him a monotherapy. And I think that's up to the discussion between you and your patient what you decide to do in the end. So then coming to my take home messages, structural damage on the group level is related to outcomes that are relevant for patients, and then you can think of spinal mobility, physical function, quality of life. But you also have to take into account that there is major variation in radiographic progression between individual patients.

So you need to know in which category your patient falls. It's important that disease activity, if you assess it by the is longitudinally associated with structural progression. If you assess it by bus dye, this is not the case. Only if you use bus dye plus CRP, then again you find this longitudinal association. So ASTHAS is an important treatment target, so you know that when you can reach a low ASTHAS, then it's also less likely that the patient will develop new damage.

The non risk factors for spinal progression is male sex, smoking, having already syndesmophyte, an elevated CRP or ASTHAS, radiographic sacroiliitis that is only in patients with radiographic axial SpA, and inflammation on MRI spine. We have conflicting results on the effect of NSAIDs on structural damage progression. It may be that there is a positive effect of selective COX-two inhibitors, but the jury is still out. We have recent trials on biological DMARDs that show less structural progression compared to the first trial of the TNF inhibitors. But I think here you need to be careful with the interpretation because this may be due to a bias in the time period that the RCT was conducted.

From the SURPASS trial we know that there's no difference between TNF inhibitors and IL-seventeen inhibitors, and reviewing all the observational data together in a special way, a special analytical technique for observational data, that analysis makes it likely that BD mass have an indirect effect via inhibition of inflammation on spinal structural damage.

Thank you, Desiree. That was great. You know, the debate for many years has always been, do you change outcomes? Is the therapy that we use in spondylitis capable of disease modification? Because the X-ray changes are so slow.

But I think Desiree's work and the work of many, as she points out, says, yes, there is a significant structural benefit to the therapies that we use. Our next speaker is Jennifer Cather. Jennifer Cather is a well known dermatologist from Mindful Dermatology in Dallas, Texas. I've asked her to speak about hidradenitis suppurativa, well known to dermatologists, and I see a lot of these patients. I think you do as well.

And is this something that you should be knowledgeable of and treating as many rheumatologists do? She's going to talk about advances in hidradenitis suppurativa.

What do we know about hidradenitis? So it's very different globally. The Western population prevalence is between one and four percent, probably underreported. Its onset is after puberty, ten percent before eighteen, twenty percent after 45, right in the middle is where we see a lot of the cases. Right in the middle is where we're really living life psychosexually, getting involved with our education, our careers.

And this is a disease that stunts that trajectory. There's a female predominance in North America, about two point five women, one men. You go over to Asia, it's about equal if not more men. The delay in diagnosis is on average of ten years. My purpose of today is to get that on your radar and to start thinking about it.

That's really what I want to know about, that you'd walk away with. There's a lot of pathophysiology with this. Remember the genetic predisposition, about forty percent of patients have a family member which is great. There's a lot of extrinsic factors. A lot of them are smokers.

I always tell people with the disease, if you keep smoking I will not clear you. There's a mechanical stress. So when I was growing up in dermatology it was always this apocrine gland problem. It ends up that it's a hair follicle plugging, you have disruption of that, you have dysbiosis, you have inflammation and then you're off to the races with all this inflammation which involves TNF alpha, IL-one, IL-seventeen. And there's an altered microbiome.

Rarely is there ever true infection unless there's a lot of open sores. So this is a lady I had when you guys got adalimumab in 2005. All of the patients in my clinic all of a sudden had psoriatic arthritis. So this lady comes in, she has psoriasis. I started her on adalimumab and this was like 2008.

And she comes back and she's super happy because I've actually helped her with her psoriasis. But she goes, that's not the best. Look at this. And she raises her arms. I never looked under her arms.

Inverse psoriasis was not really a thing back then. And she goes, it helped this. And I was like, oh wow, there's a lot of inflammation in this thing that we call hidradenitis. So this is a lady that actually has stage three hidradenitis on this side and then like stage one that two on that side. So if you think about what this lady's gone through for years, she's had weeping, odor, pain, problems with moving her arms and I have helped both.

So that's kind of exciting. I never miss that again. All right, so the diagnosis we have to have characteristic lesions in characteristic locations. And then we have chronic and recurrence. So the lesions we're dealing with are inflammatory.

They're usually painful nodules, pustules. There are sinus tracts and scarring. They're in highly dense apocrine glands place. Think of skin on skin, your neck, your underarms, your groin, your anogenital between your buttocks. And the chronic and recurrent, the clues are two lesions in the last six months or a lesion that just doesn't go away for about three months.

And then there are these different phases, inflammatory, destructive, burnt out. We really need to do better with the inflammatory and destructive. And by the time you get burnt out you're cutting it out unfortunately because they have so much fibrosis. So this is a person, so when Doctor. Cush asked me to give this lecture I go I've never given an HS lecture.

Oh my gosh. So I looked back and I looked at all of our data just in the last couple of years. And we had, these cases and I was like do I have a photo? And so I looked back and this was a person we saw on March, 2022, diagnosis and abscess, we didn't get it. 2023 comes back, we get it, it's HS.

So it has been there forever, this lesion. So it's been there a long time. This is a person that in the axilla comes in with one inflammatory nodule. Nowadays I tell people this might walk in as a painful hot nodule and you go abscess. I say it might be an abscess, I'm going to culture you and she had nothing else.

But I want you to know that there's this other thing called HS. So I don't have a dermatologic exorcism when she comes back. I give her a piece of, something in her mind to go, if this keeps happening, this dermatologist told me she can help me. Negative culture, the right, the left one rather, easy to get, right? Because you can see all the scarring.

You have this inflammatory nodule there and you're like, you have HS. The first one, I'm not sure. The second one, I've nailed it. So this is another person. Again, hard to get on the right.

A lot of inflammation, post inflammatory scarring. This other one, nodule in the groin and look at the white. That is from your intralight lesional catalog that you've done, all right. So whether you did it or they've done it, you know that this has been there before. It's important to examine multiple areas, but sometimes they won't.

What's so interesting, we always know in dermatology, Craig Lianardi taught me this, if they're in a gown they're going directly to a systemic. These people aren't in gowns. They're not ready for what you have to say. And so remember that you have to kind of meet them where they are. So this is a lady that I have, she has metastatic lung cancer.

She's a current and past smoker. She has HS and psoriasis. So remember eighty percent of HS patients are current or past smokers. It's really important to try to intervene with that. The smoking usually predates HS by four to five years.

So if you have a family with HS and you're looking at the eight year old kid of the woman with HS, this is a reason not to smoke. When they're dragging their kid to their derm appointment, don't smoke because it actually might modulate your disease. So the fistulas are very hard to deal with, and the inflammatory nodules are very painful. So this is actually another person, axilla on the right, groin on the left. The groin on the left has so much destruction when we're looking at the exam she has to hold the other labia back because there's been so much fibrosis there.

So again, hard to treat and hard to get rid of it once it gets to the scarring phase. So the comorbidities are listed here. We've got smoking, obesity, really hard to intervene with that. I'm married to an addiction psychiatrist. We've done some smoking cessation classes and we failed.

Metabolic syndrome, inflammatory arthropods, that's you guys. Inflammatory bowel disease, very important to figure that out in the family and in the person because the therapies I'm going to discuss. Depression and anxiety, probably thirty to forty percent of patients have that. PCOS, I can help with that. There's something called the follicular occlusion tetrad and it's so great.

If I could have had a picture of the dissecting cellulitis of the scalp, we know what pilonidal cysts are. And then squamous cells, so if you have a person with HS and they have an anogenital sinus tract and it's painful and you see a lesion it needs to be biopsied. Because if you see a squamous cell that's where it's usually going to be. I've seen it once. I'm 55, it's not common.

So there are these autoimmune disorders. These all go to the medical school like Artie was talking about Sappho. I can diagnose it and I'm sending it to somebody who's very interested in that. Very hard to keep all hands on deck modulating and looking at all those different things. Grading systems.

There are four or five. I choose to do the Hurley stage because it's the easiest. And this will just give you an idea when you're talking on the phone about what to tell a person they can get an idea. Hurley one nodules and abscess, minimal scarring. Two, they have limited sinuses and some scarring.

And then three, a lot of sinus tracts and a lot of scarring. I'm going to show you some of those. This is Hurley one. The reason I'm showing you these is because to get in the clinical trials for every drug thing, trial I've seen, you have to be a HIRLI two or three and that is too late in my mind. We really need to be intervening with HIRLI one or two.

So this is Hurley stage one painful abscess and this is another breast. And again this is Hurley two. This is a person I just saw last week which is super cool. So she's 29, she has a nine year history. She only gets these lesions on her neck and she also has this rash on her neck.

It ends up she has a sister and her sister has more lesions in her groin. And so I'm going to snag that sister and because her sister has multiple locations. The lady wants to know what is this on my neck and she also wants to know what is that rash on my neck. And then you look at her nails. So she's got HS, she's Hurley two and she's got psoriasis.

And those are great psoriatic nails with her PIT. So always look at the nails, very cool. This is another Hurley two, you get these pockmarked scars. This is not from extractions. This is a person with HS on her breasts and they're dripping.

So remember that these people have a huge wound care issue. A lot of these women and men wear maxi pads that they actually, take the strips off, put it on their clothes and put tight clothes on. And remember how I told you a lot of this is a hair follicle problem? The mechanical stress that does on the hair follicle, it doesn't help that much. It actually kind of hurts them.

But we got to figure out how do we bandage this? How do we wear this? It's all over the place. So this is another person with nodules and these things called tombstone comedones. So if you see two comedones kind of together, that's actually tombstone comedones.

That's almost pathognomonic for actually HS. So I told you that it's pretty rare to get an infection with HS. This is somebody who got an infection with their HS. Under their breast they've had this huge ulceration, non healing, and they had a cellulitis required IV antibiotic. So the language should be it's usually not infectious, but if you have open sores and we're not doing wound care and wound care is hard and it costs a lot of money for these people, then we need to have you come in, call and get you to infectious disease.

So our therapies, to pick the appropriate therapy you need to understand the full impact of the disease. What can't you do? What would you do if you didn't have this? You know, it changes what they wear. It changes the activities they do.

You need to educate them about healthy lifestyle changes that gets you a bad yelp every time. Reduce lesions and help with wound care. Control the odor. Odor is something that you wouldn't really think about until you've sat with them for a little bit and they take their clothes off and they're comfortable. The odor is what isolates them.

Controlling pain is hard. Dermatologists are not really great with pain management so we get them hooked up with pain management. These people wake up in pain and they go to bed with pain and they're not sleeping. Sleep disorders are an independent cardiovascular risk factor so we need to really keep our eye on that. It would be very cool if we could improve comorbidities.

And a lot of the medications we think about might do that. So this is actually from Doctor. Cush and I love it because it leads me into wound care. So if you look at this, this is an oozing mess. Okay?

So all you have to ask about is do you want to smell like a pickle or do you want to smell like a pool? So you either do vinegar water soaks and it's one to four vinegar to water and it helps dry it up and it helps their odor. Or pool, you do a tablespoon of bleach into a gallon of water. And they can actually swab that on, that's a great antiseptic and it gets rid of their odor. This is another one of his patients and it's great because it goes back to my case.

This guy has terrible inflammatory acne on his face and it's under his arm. What I find fascinating is this person in my clinic would never wear a white undershirt because of the ooze and the staining. They're usually wearing different clothes. So I really like those photos. Our therapies, so old school, antibiotics, topicals and systemics, clindamycin solution, doxy, that's kind of where you go first time if the person is not ready for the sound bite of chronic, systemic, inflammatory disease state, at least you're putting something in their mouth.

I love resorcinol, it has to be compounded. Within twelve weeks the clindamycin is actually not helpful, so resorcinol works longer. Anti androgens, whether they're birth control pills, fenestrites, spironolactone, or metformin. Retinoids are not used very much. Biologics, I'm a big biologics person.

JAK inhibitors. Laser hair removal, I have some debates about that. And then Intralesional Kenalog. Intralesional Kenalog will make you happy for two minutes and then it all comes back. But sometimes it does help with the pain.

So this goes back to the follicular component here. So I was never a big fan of laser hair removal. It's not covered. But if it really is all mechanical, frictional in some patients, this shows you if you look with your dermatoscope, there's destruction of all the hair follicles. And you can see this has been going on a very long time.

This is a lady who, she's 30, she has a family history of hidradenitis, I have her mom in my clinic. She gets in a gown immediately, she's 30. She has Crohn's disease and when I meet her she's on an Aisle 1223. She inquires about laser hair removal. I said there's some data with it.

She does it, it helps. You can see all the other inflammatory places she's had and you can see where I've done my intralesional catalog and caused terrible atrophy. But really she shouldn't be on a twelve twenty three, it failed trials. So I need to change her to adalimumab, which I do. And in my quality of life, I ask her what she can't do.

She can't sit down, she can't do her spin class, which is like a religion to her, And her sexual impact, she is not being able to get into a relationship and that really upsets her. And that is not necessarily because of the severity of the disease, it's the isolation she's had on the way to where she is now at 30. So remember, there is no such thing as a little bit of hidradenitis. It isolates you from day one. Okay, so what are the approved medications?

Not a lot. So we have adalimumab, secukinumab and most recently bimekizumab. These all were approved based on the high score, it's a validated measure. You have to have a fifty percent reduction in inflammatory lesion count, no new abscesses or fistulas. And those are the articles there that were the phase three pivotal trials.

So the only article you really need to read was the article that Doctor. Gave me I think four days ago. And it's that Lancet article, it came out February 1. And he goes, this might be interesting. I'm like, it would have been interesting if it came out like a week ago before I had to pull out all these other things.

You only need to read that Lancet article. And that is actually the thing I gave to you guys. So in the clinical trials note that the IL-twenty three targeting biologics, they failed. That should be IL-one, it failed. Bredalumab, meaningful.

A lot of oral kinase inhibitors, super exciting. And so those are the things that I wanted to pick out of clinical trials because some of those will actually get approved in

Thank you, doctor Katherine. That was great. Our final speaker today is doctor Katherine Bakewell from Salt Lake City. Katherine is a go to source on PSA spot and imaging, and we've asked her to talk about imaging and evaluation of spondyloarthritis. Take it away.

So here an overview of some of the radiographic features that we can see in psoriatic arthritis and spondyloarthritis in general. So the classic pencil in cup deformity here shown at the thumb in this patient really highlights some of the changes that are classic for spondyloarthropathy, which is a combination of bone erosion or degradation along with juxtaarticular new bone formation or bony hypertrophy and new bone deposition. Here, again, highlighted by one digit, you can see erosion, ankylosis, joint resorption. And so this is unique to the spondyloarthropathies. You will not see this in conditions like rheumatoid arthritis where you can see bony erosion and osteoporosis, but you're not going to see that new bone formation in the same plane.

So again, just a quick review. We're taking a look at the modified New York criteria for sacroiliitis by x-ray. It goes on a grade zero all the way up to grade four. So grade zero would be totally normal. Grade one would be suspicious or unclear, and that's here up in the upper left.

A grade two, you're going to see perhaps some small erosions and some sclerosis of the bone. Grade three, you're going to see definite erosions, perhaps pseudo dilation of the joint space. And by the time you get to grade four, that is an ankylosis of the SI joints. In order to qualify, you need to have either a bilateral hicraleidus grade two or a unilateral grade three or grade four. And again, this is still what we use as our classification criteria for radiographic axial spondyloarthritis or ankylosing spondylitis.

But this is: A, features that we talk about predominantly for ankylosing spondylitis and B, fairly late changes. And so as we shift on to MRI, I want to show you some earlier changes. But I do want to pause and take a moment to show you that there are radiographic differences between classic axial PSA and ankylosing spondylitis. So in axSpA or AS, we conceptualize the lesions as generally being more severe than in axial PSA. They're more often symmetric.

So you can see here this individual has a bilateral grade three sacroiliitis And at the level of the spine, you can appreciate how the syndesmophytes truly are affecting every disco vertebral unit. This is a flowing this would be the classic bamboo spine. Whereas when you get over to the axial PSA, the syndesmophytes are fewer and farther between and they have that almost waxy appearance like a candle dripping wax and more intermittent. You'll also note that the sacroiliitis is more asymmetric with one side demonstrating a grade four complete ankylosis, the other one demonstrating grade two or sclerosis here visualized without clear erosion of the joint space. And this is classic for individuals who may also have a different underlying genetic makeup.

So this would be classic for the HLA B08 phenotype and or HLA B38 but not the B27 that you see classically in AS. Now, some individuals with axial PSA may have a positive HLA B27 and they in turn will exhibit more of the classical AS morphology on x-ray. Here on this slide, my main point that I want you to take home is that spondylitis without sacroiliitis can occur in up to a third of individuals with axial PSA. So what does this mean? You get an x-ray of the SI joints and they're fine, but if you actually look, if you image the area where the patient is affected, the cervical spine, the facet joints is classic, you will indeed find changes there of ankylosis or syndesmophyte formation.

And so hence the recommendation that we consider screening the spine for axial PSA changes, even if there's no inflammation on the SI joints. And that is different, as I will show you here in a moment, from axial spondyloarthritis or AS classically. So this is a demonstration. This has been around, this figure is now twenty years old, of our conceptualization of how we can move from a non radiographic sacroiliitis or imaging inflammation only on MRI to radiographic changes. And this can take anywhere from months to years for these changes to occur.

And this is what they look like again on a time scale. We have starting at the earliest time point bone marrow edema, which is the most sensitive but least specific for axial spondyloarthritis. And then we start to get into some changes such as fatty metaplasia and then bony sclerosis and desmophyte formation, which then we have converted over to a radiographic arena since these can be seen on x-ray. The question is raised when should we be getting MRI? When should we be getting an x-ray?

And suffice it to say, I will just start with this finding from the Desir cohort from EULAR a couple of years back where they found that if you're monitoring for structural damage in axSpA, MRI is preferable at the level of the SI joint, while radiographs, the modified Stokes ankylosing spondylitis scoring system, or the MSAS, is preferable for the spine. So x-ray spine, MRI SI joints. And the reason for this is that you get too much noise. You can capture some additional inflammation with an MRI of the spine in an individual with AS. But if you were, looking specifically for diagnostic purposes or even monitoring of structural progression, the most specific is the x-ray.

You're going to get too much background from things like herniated discs or other nonspecific edema with the MRI of the spine. So what do you do when you order an MRI of the SI joints and you put this into the radiologists at your institution? They should be getting T1 weighted and STIR sequencing in a semi coronal scan of the SI joints. The most common question that I have heard from people wondering are we doing this correctly is should we be using contrast? And the short answer is no, you don't need it.

The STIR is going to pick up that inflammation in an adequate fashion and you don't have to put the patient through that extra expense and exposure. So here, this is what you see. You can see the two different sequences demonstrated: STIR on the left and T1 weighted on the right. You can appreciate how fat is dark, so you can have fatty metaplasia here on the STIR sequence, or it also consists of, you know, phrased low signal, whereas fluid or edema is bright or high signal. And of course, again, as I mentioned, very earliest signs of sacroiliitis, spondyloarthritis least specific.

And then here, when you look on the T1 weighted image, which is excellent for your anatomic changes, things like erosions, You can see the edema as low signal or dark, whereas the fat is high signal or bright. So that's how you can tell the difference between these two sequences. So in summary, you have a patient in front of you who you suspect is having axSpA with inflammatory back pain. You get an x-ray. If it is normal or if it is equivocal, you move on to an MRI, being cautious to not over interpret changes of just bone marrow edema.

But when you start to see the structural lesions of fatty metaplasia and erosions, you know you have something more specific for spondyloarthritis. And the effort has been ongoing. So this goes all the way back to 2,009. There was an effort to make a consensual approach to how do we define a positive MRI for SI joint inflammatory lesions when we talk about bone marrow edema. And the decision was made at that time that you had to have two or more bone marrow lesions on a single SI joint slice or you had to have bone marrow edema on two consecutive slices.

And then you would consider it consistent with axial spondyloarthritis. But this kept having issues. Multiple papers would show, for example, that up to twelve percent of healthy controls would have these MRI changes of bone marrow edema on two consecutive slices or multiple quadrants. And so this wasn't quite specific enough. They really wanted at least a ninety five percent specificity.

And this was further confounded when you looked at individuals who were athletes. So here we're looking at scans of people, 20 healthy recreational runners, 22 elite ice hockey players, violence sport. And in these individuals, the ASAS definition for sacroiliitis was met in about a third of the recreational runners and up to forty one percent of the elite ice hockey players. And so the decision was made, look, we really need to get more specific with this. We need to dial down.

And so I want to bring forward this effort. And you'll look at the author list. You can see this is many of the heavy hitters, if you will, in axial spondyloarthritis and MRI in particular. And they first looked at all of the different lesions and they chose only those that had at least a ninety five percent specificity for axial spondyloarthritis and then put them through additional validation of having rheumatologists follow. So if you had an individual with inflammatory back pain without a classification of axial spondyloarthritis, could these lesions have a positive predictive value again of at least ninety five percent?

And that is where this rule came forward. So we're looking at there's for each of these active inflammation as categorized here by bone marrow edema, structural lesions such as erosions, and fatty lesions. So you came up with the three, four, five rule if you're going to look at individual quadrant. So that's taking each SI joint and putting a grid over it and dividing it into quadrants. So if you see erosion in at least three quadrants, bone marrow edema in at least four, or fatty lesions in five or more, that meets classification criteria by imaging for axial spondyloarthritis.

You can do this also depending upon the number of consecutive slices that you see these lesions in. Now there is one thing that we humans do that believe it or not is even more inflammatory for the pelvis than elite ice hockey playing, and that is pregnancy and delivery. And so even when you are applying these criteria, there was one study that showed that the majority of women by twenty weeks of pregnancy will have, for example, bone marrow edema with a SPARC score of greater than four. And this starts to drop off postpartum such that by a year's time it's only twenty percent who will still meet that criteria. And so the recommendation is that we, as much as possible, try to not use MRI of the pelvis to classify individuals as having axial spondyloarthritis during pregnancy or for the first year postpartum.

Now, these have to be applied, if you're in that clinical situation, looking to your structural lesions such as erosions, still are relatively specific. So in that same series, it was only two point eight percent of postpartum women who had definite erosions on MRI at the SI joints. And so you can still see it, but you still have a relatively high specificity. So what does this look like as this progresses over time? So we've talked about how you have active inflammation and bony erosion, right?

So this is kind of the resorptive phase, but this is followed by a fibrous repair of tissue. And the last then is what we're going see is this new bone growth in syndesmophyte. So this is all in that non radiographic arena, and it's this last phase where we finally start to see changes on x-ray. And again, this process is unique to the spondyloarthropathies. Think about rheumatoid arthritis, which is characterized by a robust inflammation throughout.

Here, there's actually an inflammatory phase that appears to die out, and then this fibrous process takes over. So let's talk about our scoring systems. And I think this is particularly relevant as we're diving deeply into the differences between axial spondyloarthritis and axial psoriatic arthritis. We'll start with the oldest, the Berlin MRI scoring system for axial spondyloarthritis. This gives separate activity and chronicity scores.

And you'll notice here that erosions are under activity, kind of similar to what I showed you on the last slide where there's still a lot of inflammatory cells busy making those erosions, whereas the sclerosis, syndesmophytes, and ankylosis are going to be under that chronicity score. This was used in several clinical trials, was followed by the SPARC score which was a little bit more widely applied. I would have to say this is the one I have seen most commonly used in axial spondyloarthritis clinical trials. In the SPARC scoring system, each disc overtebral unit is broken into quadrants. Again, that grid I was referring to earlier and scored separately on depth and intensity of bone marrow edema.

You'll notice that the grid does fall over the disc, it does not over the vertebra itself. And here included, you guys all have my slides, but you can go through and play with the scoring if you like, again, looking at the depth and intensity of each of these lesions. So I brought these up because I wanted to highlight this score, the Canden scoring system. There's the question out there, could this actually be more sensitive for axial psoriatic arthritis rather than axial spondyloarthritis. And this, the can den, comes from the combination of Canada and Denmark.

Walter Miksimovich is from Canada, Mikhail Ostrgaard from Denmark. These are two of the thought leaders throughout the world in MRI of spondyloarthritis, and they have not always seen eye to eye on imaging and interpretation, scoring of these lesions. And so the CANDEN truly represented a unification, a melding of the minds on how we could look at these things. And it is different specifically because it includes these facet joints, or posterior element inflammatory lesions. So in contradistinction to the Berlin and the Spark, which really focus just on the disco vertebral unit, we now have a scoring system that's looking outside just the spine.

Thanks, Catherine. You know, I cut her off. She was going to get into a case and also discussion of ultrasound in spondyloarthritis. If you want to hear that, see that, you can go to roomnow.live and get the old content. But more importantly, register for our next meeting.

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You and 500 other people will do so. Tune in next week for our last session, which will be on vasculitis from Room Now Live twenty twenty five. Again, thanks to AbbVie, the sponsor of this program. Take care.