We shine this spotlight on Ankylosing Spondylitis (AS), a type of Spondyloarthritis. It is sometimes called Radiographical Spondyloarthritis (rSpA), because the typical bone damage or fusion is visible on X-rays. Ankylosing Spondylitis is the most prevalent of several types of chronic Spondyloarthritis disorders that cause joint pain, morning stiffness, fatigue and other chronic, fluctuating symptoms. Consequently, long-term untreated disease may lead to spinal fusion and permanent deformity. Below, we offer basic facts about this autoinflammatory arthritis that primarily affects the lower spine. Further down, links will connect you to available statistics, research initiatives, supportive patient communities and more!
The oldest autoinflammatory disease?
Ankylosing spondylitis has the dubious distinction of being the oldest autoinflammatory disease we know of. That’s because the spinal, especially sacro-iliac, fusion may be preserved in bones or fossils. There are fossil dinosaurs with characteristic hip and lumbar lesions. A 900,000 year old Miocene crocodilian from Egypt also shows typical vertebral fusion. AS lesions are also seen in fossil bones of cave bears and saber-toothed cats. Some of the Smilodon specimens from the La Brea Tar Pits show signs of sacro-iliac AS.
Thus, it’s not too surprising that Human AS has been around a long time, too. The oldest specimen is an Egyptian man from the third Dynasty period (~2900 BCE). Additional burials from Europe, Africa and South America from 400BCE to 500AD have skeletal changes diagnostic of AS. However, the disease was first described by a physician in 1691, then repeatedly spotted through the 19thC. By 1904 Frankel named it “spondylitis ankylopoietica.” The disease has gone through many different names and classifications.
Today, the consensus is that AS is a chronic autoinflammatory disease. That is, AS is a result of an overactive innate immune system (in contrast to aultimmune diseases that involve the adaptive immune system).
An overview of ankylosing spondylitis (AS)
Ankylosing spondylitis is a chronic rheumatic disorder and a systemic autoinflammatory disease. That means the patient’s own innate immune system causes chronic tissue inflammation and eventually damage. It is one of a family of inflammatory spinal arthritis diseases, collectively called spondyloarthrites, which means inflamed vertebral joints. These diseases may also have non-spinal symptoms and some of them overlap. Additional diseases in this category include Psoriatic Arthritis (PsA) (associated with the autoimmune skin disease, Psoriasis) and Enteropathic Arthritis (EA) (associated with Inflammatory Bowel Disease–IBD). Recently, a newer classification system groups these diseases as axial (central, as in the spine) or peripheral (outside the spine).
Typically, the AS disease process starts before age 40 and is focused on the lower (lumbar) vertebrae. Specifically, the hallmark of AS is chronic pain and stiffness after rest in the sacroiliac joints (sacroilitis). The sacroiliac connects the sacrum (the flat triangular bone between the buttocks) to the pelvic bones (ilia). Over time, inflammation of the connective tissue (entheses) of the spine leads to scarring and eventually formation of extra bone. If allowed to persist, it can cause fusing of the sacroiliac joint, the spine, reduced flexibility and a hunched posture. Furthermore, AS can affect other joints as well, including hips, ribs, shoulders, even the smaller joints in the hands and feet. Sometimes AS causes eye inflammation: uveitis (inflamed white part of the eye) or iritis (inflamed iris). Rarely, the disease may inflame and damage heart and lung tissue.
Akylosing Spondylitis statistics
Current available ankylosing spondylitis statistics estimate that…
- An estimated 1 in 2,000 people suffer from AS.
- Symptoms most commonly emerge in young adults.
- Men are affected seven times more than women.
- Genetic marker HLA-B27 may predispose people to spondylitis.
Symptoms include chronic low back pain, sometimes severe, back and hip stiffness (especially in the morning after sleep), reduced mobility and fatigue. Hip, rib, chest, shoulder, heel, even wrist pain are not unusual, since, as a systemic condition, it can affect many parts of the body. In some patients, eye inflammation symptoms include eye pain, blurred vision and light sensitivity. There may even be gut or skin symptoms, which will suggest a diagnosis of EA or PsA. As with most immunological diseases, the course of AS is highly variable, not only from person to person but over the course of individual patients diseases. Symptom flares and periods of remission are typical. Flare triggers include food sensitivities, stress, and lack of exercise.
Patients generally experience low back pain and stiffness after rest, which prompts them to see their primary care physician (PCP). This post has helpful advice for preparing for a doctor visit. The diagnosis process usually begins with a physical exam by your PCP. As part of the exam, your doctor will test the range of motion of your spine. If limited mobility and other symptoms suggest a rheumatological disease, your PCP will refer you to a rheumatologist for further evaluation.
Your PCP or rheumatologist may give you an assessement tool to fill out. These include questions about pain, mobility and ability to do work and paly activities. Once you are in treatment, you and your doctor may use these tools to monitor disease progress or remission.
Since there is no single test for AS, the diagnostic path should take into account family and personal history, blood lab workup and imaging. A family history of inflammatory low back pain is suggestive. So is biological family members with autoimmune diseases, especially Psoriasis, PsA or IBD. An even bigger clue is a personal history of inflammatory sacroilitis.
There is a genetic marker, HLA-B27, which can be detected on DNA testing. However, HLA-B27 positive results may not be definitive. Some 90% of white European AS patients will be positive, but the presence is lower among people of other ethnicities. Most HLA-B27 positive people never develop AS.
Other blood tests include Erythrocyte Sendimentation Rate (ESR) and C-reactive protein (CRP), levels of which are elevated in many, but not every, AS case. Finally, radiology can show gross changes in joints and bones (Radiographical Spondyloarthritis). However, if X-rays are negative (Nonradiological Spondyloarthritis), MRIs can show more detailed images of the affected parts of the spine.
Treatment and management
There is no cure for AS. Therefore, treatment aims to relieve symptoms and prevent further complications. In the first place, consistent regular exercise is essential to maintain mobility and prevent deformity. Active physical therapy can help with flexibility in the spine and overall posture. Other movement therapies may help, too.
However, medications may be necessary to treat pain and stiffness. Firstly, nonsteroidal anti-inflammatory drugs (NSAIDs) can relieve inflammation and thus pain and stiffness. The preferred biological or specialty medicines are Tumor necrosis factor (TNF) blockers that can relieve swollen or tender joints. Sometimes, steroid injections are used. Moreover, a variety of alternative, complementary, or functional treatments may be integrated with conventional treatment. These include massage (although it may be a trigger in some patients), acupuncture and yoga.
Certain foods and food components may help manage AS symptoms. Some patients may have food sensitivities as well. This is especially likely in people with gut symptoms or a diagnosis of IBD. Maybe the gut microbiome is a mediator of these effects. In any case, check our YAC Food Spotlight on Ankylosing Spondylitis.
While the Spondylitis Association of America, and other organizations work toward raising awareness and improving care, our team at Your Autoimmunity Connection connects patients with one another and with currently available resources.
Brush up on the basics
While some of you may already have some background knowledge about ankylosing spondylitis, let’s take a moment to review the basics. The following pages provide a comprehensive overview of AS:
- Spondylitis Association of America: Overview of Ankylosing Spondylitis
- Read about symptoms, diagnosis, risk factors, causes, and more.
- National Ankylosing Spondylitis Society: Resources
- Check out these various patient guides, from managing your flares to reducing fatigue.
- Mayo Clinic: Ankylosing Spondylitis
- Learn more about complications, medications, and lifestyle remedies.
- Medical News Today: All About Ankylosing Spondylitis
- Explore an interactive 3-D model of what spondylitis looks like in the body.
Find your patient community
- Spondylitis Association of America: Connect With Others: You Are Not Alone
- Connect to online or in-person support groups, or read stories of others suffering from spondylitis.
- Drugs.com: Ankylosing Spondylitis Support Group
- Ask questions (or answer them) about medications related to spondylitis.
- Daily Strength: Ankylosing Spondylitis Support Group
- Create your own post or read others’.
- Facebook groups & forums
Research and Clinical Trials
- Spondylitis Association of America: Research
- Check out this database of research articles, or participate in current research studies.
- CenterWatch: Ankylosing Spondylitis Clinical Trials
- Browse clinical trials that are happening right now.
- Nature: Latest Research and Reviews
- Explore the latest studies on ankylosing spondylitis.
Ankylosing spondylitis is an autoinflammatory disease
In conclusion, to look at the bigger picture, we must remember that Spondylitis, including AS, are chronic inflammatory or autoimmune conditions, of which there are more than 100 individual diagnoses. According to our research, some 50 million Americans suffer from one or more autoimmune diseases. One research study further estimated that approximately 25% of patients with autoimmune diseases have a tendency to develop additional autoimmune diseases.¹
We hope our spotlight on ankylosing spondylitis connects you with useful resources and information. We believe it is essential to take a holistic approach to combat the autoimmune disease epidemic. By looking at all autoimmune and inflammatory diseases together, we can move away from the fragmented view that hides the magnitude of the problem. Rather, we would head toward concerted action in reshaping research, diagnosis, and treatment. Our model is based on the revolution in cancer research and treatment over the past 50 years. This was only made possible by viewing cancer as a group of diseases with a common foundation, thus garnering far more resources than had been devoted to individual types of cancer alone. Help us bring this revolution to autoimmunity!
Written by: Bonnie Feldman, DDS, MBA, Anna Simon, Ellen M. Martin
Why autoimmune and autoinflammatory disease?
Autoimmune disease is an “invisible epidemic.” Despite affecting roughly 16% of the US population (as many as cancer), autoimmune and other chronic inflammatory diseases remain under-recognized, under-researched and under-served. In order to raise awareness and connect patients, families and caregivers with useful resources, we at Your Autoimmunity Connection publish this series of “spotlights” on autoimmune diseases.
Chronic inflammatory diseases are high-beta, high-risk and high-cost to payers and providers, especially for employer-sponsored health care benefits programs. Therefore, these spotlights offer useful background for benefits managers and digital entrepreneurs building companies and products addressing these diseases.
Get acquainted with Your Autoimmunity Connection
- Check out our blog at www.drbonnie360.com for all things autoimmune – from updates in research to possible lifestyle modifications, patient stories, and more.
- Find us on Facebook here, or join our Facebook Forum to connect with patients across all autoimmune diseases.
- Read our Guide to Food Therapy
- Check out our other disease Spotlights here
 Cojocaru, M, Inimioara Mihaela Cojocaru, and Isabela Silosi. “Multiple Autoimmune Syndrome.” Mædica 5.2 (2010): 132–134. Print.