Ankylosing spondylitis (AS) is a chronic inflammatory disease of the axial skeleton, manifested by back pain and progressive stiffness of the spine. Characteristically, it affects young adults with a peak age of onset between 20 and 30 years, however an untreated disease may be also diagnosed in the mid 40 to 50 years of age. The name for the disorder is derived from two Greek words: "ankylos", which means bent or crooked and "spondylos", which refers to a vertebral bodies or the vertebral column. The term "ankylosis" therefore refers to a fibrous or bony bridging of joints. In the spine this includes bridging of one or more intervertebral bodies. In the sacroiliac joints (SI joints) the inflammation and fibrosis may produce high pain at the connection level of sacrum (tail bone) with the Ilion (pelvic bone). Hips, knees, ankles, as well as big tendons like Achilian tendon are frequently involved in the disease progression. In addition, other organs, such as the eyes, lungs, and heart, can be affected. AS is one of the spondyloarthritides (SpA) which show inflammation around the enthesis (the site of ligament insertion into bone) and an association with the human leukocyte antigen gene named HLA-B27. Other forms of spondyloarthritis include reactive arthritis, psoriatic arthritis, juvenile spondyloarthropathy and the axial arthropathy associated with inflammatory bowel disease.
As with any chronic inflammatory disease, patients with AS may have fatigue and malaise. Disturbed sleep, caused by back or joint pain at night, as well as an excess of cytokines release from the overactive immune cells may contribute to the fatigue. Fever is an infrequent but not absent manifestation of AS in adults. Low back pain in the vertebral area (cervical thoracic, lumbar) or SI joints are most frequently present, sometimes with an unbearable intensity. Chostochondritis (rib cage pain) with a limited chest expansion, hip, knee, ankle, shoulder pain, feet pain associated to plantar fasciitis and inflammation with pain in different tendons (tendonitis), muscle fascia (fasciitis) and periarticular bursa (bursitis) are also frequently present. Most of the patients are unable to bend down below the level of the knee because of the loss of spine mobility (Shober test); the Si joints and the lumbar spine are very sensitive at local compression or by legs bending (Patrick sign); in the advanced forms of disease, do to the loss of cervical spine mobility, the standing patient along the wall is unable to touch the wall with the head (“occiput to wall” test). The imaging techniques which have been used to assess the SI joints include scintigraphy, ultrasonography, plain radiography, conventional tomography, computed tomography and MRI. X-rays of the lumbar spine and SI joints are able to identify fibrosis, extra-bone formation or bony erosions only in the advanced forms of disease (Stages III and IV) when the joint mobility is already compromised. Therefore the initial imaging changes (Stage I of disease) are seen by MRI (bone marrow edema) or by Echo-Doppler ultrasonography (new vessel formation in the cortical bone) which are now highly recommended for an early detection of AS.
Exercise and medications are the two major options of AS treatment.
- Exercise - home-based or supervised exercises by physical therapy programs, can help maintain the function and relief the symptoms, however cannot stop the progression of the disease. Exercises include postural training, range of motion stretching and recreational activities; swimming and other types of hydrotherapy (hot tub bath) or aquatic pool therapy, are highly recommended. In addition, pain relief measures such as local heat or cold can be given a trial. At a minimum, patients with AS should participate in an unsupervised home-based exercise program including stretching/relaxing movements of 10 to 15 minutes duration, twice a day, preferably in the morning and evening.
- Medication - Nonsteroidal antiinflammatory drugs (NSAIDs) are efficient in 70 to 80 percent of AS patients who report substantial relief of their symptoms. NSAIDs should be the first line of treatment for all symptomatic AS patients. Analgesic medication may offer temporary relief from the pain, (especially during the acute attacks), but do not stop, prevent or reverse the course of the disease. Steroid therapy with prednisone and other cortisole derivatives is not efficient in AS, unless it is locally injected in the SI space or other affected joints.
- Disease-modifying agents (DMARDs) - Prior to the discovery of the highly usefulness of anti-TNF therapies in AS, the disease-modifying agents had been demonstrated to be useful in blocking the progression and sometimes reverse the course of AS by reducing the chronic inflammation which is responsible for the disease progression and tissue damage. Sulfasalazine, Methotrexate or Leflunomide may be used before starting an anti-TNF agent, with moderate expectations to control the disease. Their use is similar and had the same scientific rational as the treatment of rheumatoid arthritis. However, the association of DMARDs with anti-TNF agents had an impressive efficacy not only in controlling the progression of the disease, but also in reversing its course with some partial or total recovery of the joints mobility.
- Anti-TNF Biologic Medications – including Infliximab (Remicade), Adalimumab (Humira) or Etanercept (Enbrel) - are the state-of-the art, highly recommended therapeutic agents for AS, because of their efficacy in both stopping the progress and promoting the recover from AS disease which, if untreated, has such a high potential of rapid progressive disability. Their use and the scientific rational are similar to that of the rheumatoid arthritis treatment.