Know Your Pathology: Ankylosing Spondylitis

In the second blog as part of the ‘Know Your Pathology’ series, I will look at Ankylosing Spondylitis (AS). This is a common condition of the vertebral column in which osteophytes develop at the intervertebral space as spurs or as complete bone bridges uniting the vertebral bodies. They develop on the ventral and lateral sides of the vertebral bodies, but may also be found projecting dorsolaterally into the vertebral canal, although these are small and less common. The synovial and cartilaginous joints are affected and erosion and fusion of some of the joints, especially the sacro-iliac joint, occurs; involvement of the sacro-iliac joint is considered to be the hallmark of AS. As the spine fuses, the bodies remodel and their normal shape is lost; the ultimate appearance is smoothing and squaring of the vertebrae or the ‘bamboo spine’.

A progressive, inflammatory disease of unknown aetiology, AS in humans has been associated with the HLA-B27 antigen, found in the blood of up to 95% of Caucasians with the condition. People with AS are at risk from passing the gene to 50 percent of their children; and then the children have a 30 percent risk of developing AS. It affects males predominantly with a male to female ratio of 5: 1, with an age of onset of between 15 to 35 years of age. It is seen commonly in Caucasians and native American populations but rarely in Japanese or African groups.

This condition is common in bulls, pigs and dogs, but is also seen in other species, if less often, and is a disease of some antiquity. It has been described in two crocodiles, one from Egypt and one from Cuba, dating to the Miocene and Pliocene periods respectively. Numerous other prehistoric animals have been described with spinal lesions similar to AS, including the dinosaurs Diplodocus and Polacanthus foxi, the cave bear Ursus spelaeus and the sabre-toothed tiger Smilodon californicus. The mummified remains of animals from Ancient Egypt also show evidence of this condition, whilst descriptions by the fifth century neurologist, Caelius Aurelianus, and Hippocrates also refer to afflictions that could well be AS in humans.

It is possible that many cases of AS in archaeological human populations are not being diagnosed because of the problem of differentiating between AS and Forestier’s disease (also known as Diffuse idiopathic skeletal hyperostosis, or DISH). However, several features can be used to distinguis the two from each other, and from rheumatoid arthritis and psoriatic arthritis. AS has significant erosions of the synovial and cartilaginous joints of the axial skeleton. PA, however, involves the synovial joints of the appendicular skeleton and the cartilaginous joints of the axial skeleton, whereas both promote erosion and repair of the entheses involved. Bony profileration and fusion with no osteoporosis characterises PA and AS, and in RA the cartilaginous joints may or may not be affected. Therefore, if a complete skeleton is available for analysis, it should be possible to differentiate these erosive arthropathies.

This condition has also been reported upon under the following names: spondylosis, spondylosis deformans, ankylosing spondylosis, Bechterew’s disease, Marie-Strumpell’s disease, Morbus Bechterew-Marie-Strumpell, pelvospondylitis ossificans, rheumatoid ossifying pelvispondylitis, rheumatoid spondylitis, bamboo spine, poker back, spondylitis ankylopoetica, spondylitis deformans, atrophic spondylitis… and others.

References:

Jubb, K. V. F., Kennedy, P. C., and Palmer, N. 1993. Pathology of Domestic Animals. 4th Edition. Volumes 1, 2 and 3. London: Academic Press.

Roberts, C. and Manchester, K. 2005. The Archaeology of Disease. 3rd Edition. Stroud: Alan Sutton Publishing Ltd.

Spencer, D. G., Sturrock, R .D., and Buchanan, W. W. 1980. Ankylosing Spondylitis: Yesterday and Today. Medical History 24: 60-69

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6 responses to “Know Your Pathology: Ankylosing Spondylitis

  1. Archaeozoo – thanks very much for posting such an exhaustive account of AS – a very odd condition indeed, imo, which I’ve seen described as an auto-immune illness, where the body is effectively attacking itself, though why it should feel compelled to do so is a mystery. Although I’m familiar with the name of the HLA-B27 antigen, I’m somewhat hazy about what it does.

    One thing that really surprised me was that AS isn’t confined to humans – and what surprised me even more is that it’s been around since the Miocene and Pliocene – which seems a very long time for a disease to ‘live’ – does that mean it’s been passed down in a direct line since those times, or has it cropped up here and then in different and unrelated species over the course of time.

    Also strange that it should affect mainly Caucasians and Native Americans, but not so many African or Japanese people – I think I read somewhere that the highest rate per capita is Norway – or maybe it was Scandinavia in general.

    It takes 2 or 3 years from onset to diagnose – or maybe that process has now speeded up – it’s easier to tell after a patient has had AS for a few years, as a layer of calcium on the bones can be seen clearly on an x-ray – but surprisingly, it doesn’t always cause the expected damage to bone, no matter how badly they may feel affected.

    There are a couple of potentially dangerous side-effects from AS as well – if someone gets it and their spine sets so they’re constantly leaning forward, this can apparently cause internal organs to malfunction as they are being pushed and squeezed by the body being ‘out of position’ – not sure of the correct terminology.

    Another rarer side-effect is to the eyes – something called iritis, where the eyes can become inflamed, and if not treated immediately, can go on to cause blindness in the patient, although thankfully that seems to be a pretty rare occurrence.

    Notable too is the cluster of very similar pathologies that have such similar symptoms, which you describe in your post – in between them all, there must be a fair few million people across the planet with many of the symptoms described above – I wonder how medicine will go about curing or eradicating these illnesses – doctors sometimes advise patients that AS burns itself out quite early in life, i.e. in the 30s and 40s, but I’m not sure about that.

    But at least the treatments have improved in the past decades – before it was customary for some patients to be encased in plaster for weeks or months to restrict mobility, which made the patient much worse – whereas one of the key recommendations these days is to adopt a vigorous exercise regime, or to remain as mobile as possible during the course of one’s everyday life – for example, swimming and hydrotherapy courses are often undertaken by patients – but the odd thing about AS is that even if one does a load of exercise, as soon as that exercise ceases, the body starts to set like cement in the hours after exercise has taken place – very odd.

    I’m not sure what the prospects are for preventing or curing AS or the other similar conditions – maybe there’s something like a genetic ‘master switch’ that will one day be identified and used to control AS, or prevent it from booting up in the first place.

    Anyway, a very interesting article, and thanks again for posting it.

  2. Tim, I’m glad you found the blog interesting. AS does appear to be a condition of some antiquity, but that appears to be the case for a number of arthropathies. Whether the aetiology is always the same, or whether what we have is a case of similar symptoms but different reasons, I’m not 100% certain myself. As you can see from the blog, there are a lot of different terms being used for what is essentially the same disease, and there are other diseases which it can be confused with. That doesn’t exactly aid clarity. However, as a number of pathologies do affect both humans and animals, I see no major objection to this being another such. If someone has evidence otherwise then I’d be fascinated to hear about it.

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  4. I’m a simple guy, I think I have AS. First diagnosed at 19 for 2 years and then the diagnosis was negated. Currently 39 having chest pain 4-5 areas of uptake on my latest bone scan. I have an appointment in about a week to discuss whether I have AS or Ruematoid(sp) arthritis. How can I help my physician correctly diagnose my condition. I believe I understand what AS is and how it occurs, my guess is my back is fused to about my 8th rib. What are the stages that I can expect. I have a fairly specific goal to live to be at least 137 and this seems to be my highest most challenging health concern.

  5. Sonarmark, I can understand your concerns. However, I would like to stress that my interest in this topic is from the point of view of an archaeologist studying bones and those diseases present on them. I am not a doctor and would never claim to be in a better position to diagnose diseases than someone who has had medical training. Your physican is going to be able to do so much better than me, particularly as he has access to your medical records.

    To answer your question a little, however, I will give a brief description of Rheumatoid Arthritis, which you can compare with the information on AS in the blog.

    RA is a chronic inflammatory disease of the connective tissue and has both adult and juvenile forms. It is classified as an autoimmune disease (i.e. an individual develops antibodies to their own body tissues). What starts this response is unknown, but it does appear to be more chronic in colder climates and with specific diets (e.g high proportions of red meat and red wine). There also appears to be familial predisposition in over 60% of cases.

    RA affects multiple synovial joints symmetrically, especially the small joints of the hands and feet, wrist, elbow, knee, shoulder and neck. Less commonly affected are the ankle, hip and sacro-iliac joint (part of the pelvis). The tissue in the joints thickens and becomes granular. This eventually destroys the cartilage of the joint and damages the bone underneath. Joints become swollen, stiff and – in later stages – deformed. Fusion of joints is less common than in similar joint diseases.

  6. Thank you for your extensive and appropriate response. My apoligies for my confusion.

    I had some tests in a catscan/mri type machine which confirmend extensive bone growth(activity) through my spine and a blood test confirmed that I have the genetic marker for it. Fortunately there are immune suppresent drugs which have dramtically reduced my pain and even increased some of my mobility. I have some fusion but it is confined to my sacro-iliac joint and my lower vertebrae. The inflamation and pain stop once the bones are fused.

    Anyway, Thanks again and if you are interested in viewing my WPblog it is at http://sonarmark.wordpress.com/ Have a great day

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