Untreated AS can lead to fusion, but its been 20 or more years since that has been an issue. IF fusion occurs it starts in the neck. Sacrolitis is a fairly common condition and is determined to be related to PsA not from imaging but from physical exam with all five of the following:
Schober Test: Limited motion in the lumbar spine is symptomatic of AS. The Schober test measures the degree of lumbar forward flexion as the patient bends over as though touching their toes. Progressive loss of spinal motion is correlated with x-ray findings.
Gaenslen Test: Sacroiliac pain is often found in the early stage of AS. Gaenslen’s maneuver, another name for the Gaenslen test, stresses the sacroiliac joints. Increased pain during this maneuver could be indicative of joint disease.
Chin-Brow Measurement: This is a method used to measure the spine’s curve in the neck. Patient with AS often have necks that angle forward sharply as the spine stiffens. If the doctor is going to use the chin-brow measurement to monitor your angle, the first time he or she takes the measurement will be called your “baseline.” After that, the doctor will compare each successive chin-brow measurement to the baseline to see if the angle is getting worse.
Chest Expansion: When ankylosing spondylitis affects the mid-back region (thoracic spine), normal chest expansion may be compromised. The amount of chest expansion is measured from deep expiration to full inspiration. Measurements significantly less than one inch, which is normal chest expansion, could indicate AS.
Range of Motion: To test how well and far your joints allow you to move, the doctor measures the degree to which you can perform movements of flexion, extension, lateral bending, and spinal rotation. Asymmetry may also be noted.
Sacrolitis is as I said a very common condition effecting over 80% of the population at one time or another. It is usually related to age, injury, osteoarthritis etc and not often “disease” which is why the physical exam is critical to see if there are other factors
Imaging is nothing fancy. The most common (and acurate) are plain old X-rays:
Characteristic bilateral sacroiliac (SI joints) changes may appear as blurry erosions (wearing away) or hardening/thickening of fibrous tissue (sclerosis) on either side of the joint(s). They really don’t concern themselves with soft tissue changes as those are indicitive of other issues at this point.
Loss of cartilage spacing in the facet joints, which can fuse and become indistinguishable.
Natural spinal curvature lost and presentation of abnormal kyphosis (humpback) and/or lordosis (swayback).
Spinal fractures anywhere in the spinal column. A CT Scan or MRI may detect epidural bleeding common following spinal fracture. This bleeding may cause a semisolid swelling (hematoma), causing compression of neural elements. Fractures may lead to neurologic deficit and/or spinal deformity
Lumbar vertebrae (low back) may appear abnormally square from erosion that has occurred where bone meets fibrous tissue during the inflammatory phase.
“Bamboo Spine” is typical of ankylosing spondylitis and results from ossification of the annulus fibrosus (outer portion of the intervertebral disc—the cushion between your vertebrae), the ligament that runs along the front of your spine, and bony bridges that form across the intervertebral spaces. Over time, the spine may start to look like one, long bone; that is Bamboo Spine.
They may but not always do a CT scan or MRI to evaluate bone and soft tissues (eg, the spinal canal) in greater detail depending on the x-rays.
FWIW the classification system you are referring to for PsA has been replaced several years ago to basically 2 types of spondyloarthropathies: Axial and Peripheral.
Blood work is also important in diagnoses. HLA B-27 is one of the tests. This is a funny one. A positive test is pretty meaningless. BUT 90% of AS patients are HLA B-27 positive BUT 7% of the population is positive and of those only 6% have AS. The only result with this test that really matters is a negative
One other thing while you may well have Axial arthritis, unless you are male and under age 30, chances are VERY SLIM that you have actual AS that cause fusion etc. There is a certain population that for reasons I don’t understand seem to dominate the internet with their version of AS that is really just a form of seronegative arthritis. They seem to take satisfaction in having a “name” (and a very active fund raising foundation)
Can you clear up some confusion for me about the HLA B-27 test? A few years ago when my PsA diagnosis was first suspected, I had the test for this gene. It came back negative. Does this only rule out ankylosing spondylitis, or is it supposed to be positive in PsA cases too? Any clarification you can provide is wonderful. I don’t have any of the usual signs of AS, though my back gives me loads of trouble. I am severely hypermobile in my lumbar spine though, much of which has been attributed to ligament stretching/damage from a car accident 20+ yrs ago, and then pregnancy 11 yrs ago. Regardless of this gene, I was pretty sure I didn’t have AS. I still have issues accepting the PsA diagnosis because of a lack of psoriasis. I’m seronegative too. Overall, the only thing that seems to fit is a “seronegative inflammatory arthritis.” I pretty much thought my Dr threw me into the PsA category because NOTHING else fits. I’m a scientist and have just been struggling with the lack of concrete data to support the diagnosis. I think a lot of us have this problem.
I can only speak of my experience - it is similar to yours. I have seronegative polyarticular spondylathritis… I am HLAB27 negative.
My disease symptoms include almost all joints, but the worst are axial (spinal) and large joint. I had very mild psoriasis in two patches, about the size of a 50 cent coin, about the time of onset. I interpreted all of these things together (particularly the negative HLAB27) to mean that I am unlikely to get frank AS (meaning it’s unlikely my spine will fuse), but that I do have a type of axial PsA.
I also have enteric problems, which are not typical enough of Crohns to be diagnosed with it, but have a number of common features. Crohns and PsA have a number of gene mutations in common. My Rheumy essentially believes that I don’t have a typical version of either, but have enough of both genes that I sit in a spectrum (like a solid solution if it were chemistry), between one and the other.
Many autoimmune and inflammatory disorders seem to have this overlap, which I understand is the reason why definitive diagnosis and disease course can be so elusive.