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Bechterew’s (Strumpell-Marie) Disease or Ankylosing Spondylitis

Irina Alexandrovna Zborovskaya – doctor of medical sciences, professor, head of the department of hospital therapy with the course of clinical rheumatology of the doctors improvement faculty of Volgograd state medical university, deputy director for scientific work of the State institution “Research and development institute of clinical and experimental rheumatology” of the RAMS, head of the regional Osteoporosis Center, presidium member of the Association of rheumatologists of Russia, member of the editorial boards of the magazines “Scientific and practical rheumatology” and “Modern rheumatology” Definition. Bechterew’s disease or ankylosing spondylitis is a member of a group of rheumatic diseases that affects the spinal column known as “seronegative spondylarthritis”. Ankylosing spondylitis is a chronic, inflammatory rheumatic disease that causes inflammation of the spinal joints (vertebrae), perivertebral tissues and sacroiliac joint. The chronic inflammation of vertebrae can eventually cause ankylosis of intervertebral joints and calcification of spinal ligaments. Epidemiology. The incidence of ankylosing spondylitis has been estimated 1:1000 (one case per thousand people). Prevalence of ankylosing spondylitis parallels the prevalence of HLA-B27 gene in the general population and prevalence of ankylosing spondylitis in certain geographic locations. HLA-B27 antigen occurs in 7% of white Americans and in 90% of individuals with ankylosing spondylitis. The gene which codes HLA-B27 antigen is found in chromosome 6. HLA-B27 antigen does not effect the extent of the disease severity. Sex. Ankylosing spondylitis occurs as frequently in men as in women considering sacroileitis as a diagnostic criterion of the disease. However, symptoms of the disease are generally milder among females. Peripheral joints are most commonly involved in females than in males. Genetic predisposition. Families of patients with HLA-B27 antigen have a higher disease incidence which amounts to 20% of all cases. Concordance rate of ankylosing spondylitis among monozygotic twins is about 50%. These findings testify to the fact that not only HLA-B27 antigen but also some other genes and environmental factors play a significant role in pathogenesis of ankylosing spondylitis. Aetiology. The exact cause of ankylosing spondylitis remains unknown. However, it has been demonstrated that ankylosing spondylitis tends to run in families. A specific HLA-B27 histocompatibility antigen occurring in 90-95% of individuals is also of great importance. Infections may be also a factor. There is evidence for a possible role of Klebsiella and some other species in the development of peripheral arthritis in patients with ankylosing spondylitis. Evidence for the development of intestinal inflammation and dysbacteriosis of varying extent of severity in patients with ankylosing spondylitis is supported by research findings. Cold exposure and spine injury may also trigger the disease. Pathogenesis. Pathogenesis of ankylosing spondylitis has not been well studied. Receptor theory considers antigen as a receptor for damaging factor (for example bacterial antigen, virus, etc.) which causes a disease. Another theory is arthritic peptide theory. According to arthritic peptide theory, an increased immune response to bacterial peptide develops due to combination of peptide with HLA-B27 antigen. HLA-B27 antigen molecules act as receptors for microbial (for example, Klebsiella pneumonie) and some other triggering factors.  The complex which is formed stimulates the production of cytotoxic T-lymphocytes which are able to damage cells and/or tissues having the molecules of this antigen. In HLA-B27-postitive carriers effector CD8+ response which is necessary for elimination of bacteria is decreased, while CD4+ T-cell immunopathologic response is increased. According to antigen mimicry theory, receptor similarity between HLA-B27 antigen and microbe antigen may contribute to their prolonged persistence in the body of the patient and stimulate the development of an autoimmune process. HLA-B27 peptides do not normally attract T-cells. However, in  presence of bacterial peptides which cross-react with them they are typically presented by molecules of the major histocompatibility complex class 2 T-cells and are targeted by T-cell autoimmune attacks. “Leakage of antigen material” theory, especially of lipopolysaccharides, also exists. Antigen material of lipopolysaccharides usually penetrates through the intestinal wall into the bloodstream due to increased intestinal permeability in patients with ankylosing spondylitis and it is transported to the joints, including sacroiliac joint, cartilages and ligaments. Pathomorphology. In ankylosing spondylitis “cartilage” joints rather than “synovial” ones are typically involved. They include sacroiliac joints, small intervertebral joints, sternoclavicular and sternocostal joints, symphysis. Sacroiliitis is a typical early manifestation of ankylosing spondylitis. At the initial stage of the disease granulations which contain lymphocytes, mast cells, macrophages and chondrocytes occur in the subchondral part of the bone. Destruction of cartilage occurs slowly. First articular surfaces are sclerosed. Then fibrous and bone ankylosis of sacroiliac joint typically develops. The articular space usually becomes narrow and ultimately disappears. Enthesitis, that is inflammation of tendons generally where they attach to bone, ligaments, fibrous part of intervertebral discs and articular capsules, is also typical of ankylosing spondylitis. Inflammation and erosions are typically seen in the foci. In the course of the disease tendons and ligaments are often ossified. Cartilage and fibrous tissue of ligaments and intervertebral discs are most commonly involved. Fibrous tissue of articular capsules of intervertebral joints are less commonly affected. Spine inflammation and granulation typically occur at the junction of the fibrous ring of the intervertebral disc and vertebral body. External fibers of the fibrous ring are destroyed and replaced by bone tissue which causes formation of bone bridges between vertebrae known as syndesmophytes. Formation of syndesmophytes stops as soon as the intervertebral disc is ossified. The process typically spreads upwards, and radiographic abnormalities of the spine usually resemble a bamboo stick. Along with these changes, diffuse osteoporosis, inflammation and destruction of vertebral bodies at the junction of the intervertebral disc and square-shaped vertebral bodies are often seen in ankylosing spondylitis. Proliferation of the synovial membrane of intervertebral joints causes destruction of the cartilage of articular processes which sometimes results in bone ankylosis of these joints. Proliferation of the synovial membrane infiltrated by lymphocytes typically results in peripheral joint involvement. Subchondral granulations and erosions of the cartilage are usually found in the centre of the articular surface. Proliferative synovitis which is less common, may result in pronounced fibrosis of the synovial membrane of the articular capsule.  Proliferative synovitis may also predispose to ossification and ankylosis, destruction of the articular cartilage and bone erosions. Classification. According to the course of the disease, ankylosing spondylitis may be: 1        Slowly progressive 2        Slowly progressive with exacerbations of the disease 3        Highly progressive (within a short period of time it may lead to complete ankylosis) 4        “Septic” type (it is characterised by an acute onset of the disease, excessive sweating, chills, fever, visceritis, erythrocyte sedimentation rate (ESR) is typically 50 – 60 mm per hour and even more). The following stages of ankylosing spondylitis are singled out: The 1st stage is initial or early. It is characterised by moderate limitation of the range of motion of the spine or affected joints; X-ray abnormalities may be absent or may indicate irregular surface of sacroiliac joints, foci of subchondral osteosclerosis, widening of articular spaces. The 2nd stage is characterised by moderate limitation of the range of motion of the spine or peripheral joints; narrowing or ankylosing of spaces of sacroiliac joints, narrowing of intervertebral articular spaces or signs of ankylosis in spine joints. The 3rd stage is late. It is characterised by  marked limitation of the range of motion of the spine or large joints due to ankylosis; bone ankylosis of sacroiliac joints, intervertebral and costovertebral joints associated with ossification of the ligamentous apparatus. The following degrees of disease activity are singled out:
  1. Minimum (It is characterised by slight stiffness and pain in the spine and joints of extremities in the morning; ESR is usually 20 mm per hour, C-reactive protein (CRP) +).
  2. Moderate (It is characterised by persistent pain in the spine and joints, morning stiffness usually lasts for some hours, erythrocyte sedimentation rate is 40 mm per hour, C-reactive protein ++).
  3. Severe (It is characterised by severe persistent pain in the spine and joints; joint stiffness typically lasts all day long; exudative changes in joints, subfebrile body temperature, visceral manifestations are often seen; ESR is more than 40 mm per hour, C-reactive protein +++).
According to the extent of joint dysfunction, the following changes are singled out: I – changes of spinal curvature, limitation of the range of motion of the spine and joints; II – marked limitation of the range of motion of the spine and joints (due to limitation of the range of motion the patient has to change his job (3rd disability group); III – ankylosis of all parts of the spine and hip joints which causes complete loss of work capability (2nd disability group), or the patient is limited in ability to perform usual self-care (1st disability group). Clinical manifestations. Spine and joint involvement. Symptoms of ankylosing spondylitis usually begin between ages of 20 to 30. Ankylosing spondylitis develops slowly. Malaise, loss of appetite, weight loss, fever, weakness and fatigability may precede early symptoms of ankylosing spondylitis. One of the earliest symptoms of ankylosing spondylitis is pain and stiffness in the lumbar part of the spine or, less commonly, in the thoracic part of the spine. Pain is usually intermittent but it often aggravates, especially at night. Pain can be relieved with the help of physical exercises and  thermal procedures. Sometimes pain is the same as in radiculitis, however, it is less severe. It usually aggravates at rest and is relieved on walking. Stiffness in the lumbar part of the spine is often seen. Sometimes the first symptoms of the disease include acute short-term pains in the loin, sacral bone, buttocks and hip joints which increase when coughing, sniffing, going by public transport, etc. At the earliest stage of the disease one of the sacroiliac joints may be involved. However, after 3 – 5 years bilateral involvement typically develops. Initial symptoms of sacroileitis are not enough to diagnose a disease. Radiographic studies are most helpful in establishing a diagnosis. The radiographic studies typically include radiographs of sacroiliac joint, magnetic resonance imaging and computed tomography scan, scintigraphy with radioactive technecium. The inflammatory process spreads slowly over the spine. Involvement of the thoracic part of the spine is characterized by pain irradiating to the ribs. When the cervical part of the spine is involved, the main complaints of the patient are limitation of the range of spine motion and pain when moving the head. The patient cannot touch his breastbone with his chin.   In some patients pain and stiffness in the loin are often associated with pain in bones. The patient often feels pain in costovertebral and costoclavicular joints, transverse processes of vertebrae, iliac crests, greater trochanters of femurs, ischial tuberosities, tuberosities of shin bones and heel bones. Pain usually aggravates on palpation. Straining and rigidity of paravertebral muscles typically develop as a response to an inflammatory process in the spine. Progressive limitation of the range of spine movements leads to its complete immobility. The most common and characteristic sites of enthesitis are the insertion of the Achilles tendon on the calcaneus and the insertion of the plantar fascia on the calcaneus. Hip and shoulder girdle involvement is typical of ankylosing spondylitis. These joints are usually involved over time and in an asymmetric pattern. Hip and shoulder girdle involvement usually results in ankylosis. Other joints, including the joints of lower extremities, may be involved and, if so, in a monooligoarticular pattern. Other peripheral joints are uncommonly involved. Peripheral joint disease occurs in 10 – 15 % of patients. In about 10% of patients the earliest symptom of ankylosing spondylitis is neuralgia of sciatic nerves characterized by absence of paresthesia and other signs of nerve root involvement as well as by alleviation of pain when moving and aggravation of pain at rest. Internal organ involvement. Eye involvement. Anterior uveitis, iritis and iridocyclitis usually occur in 20% of patients. In some patients they may be the first symptoms of ankylosing spondylitis. Sometimes attacks may recur. Iritis (iridocyclitis) is typically seen in patients with ankylosing spondylitis and involvement of peripheral joints. Iritis is usually unilateral, with symptoms of a painful red eye with photophobia and increased lacrimation. Cardiovascular involvement occurs less commonly, and it is highly variable. Cardiovascular involvement may include aortitis, myocarditis, pericarditis and myocardiodystrophy. Clinical symptoms are usually unclear. Myocarditis is typically associated with atrioventricular block of varying extent. In ankylosing spondylitis isolated aortic valve insufficiency may be caused by inflammatory changes either in the aorta with its subsequent dilation or in the cusps. Aneurysm of the ascending aorta and the superior part of the descending aorta is likely to occur. Young adults may develop acute aortitis and disorder of the myocardium function. Fibrosis of the subaortic part may cause disorder of impulse conduction and even complete transverse block. Pulmonary involvement occurs less commonly. Restrictive lung disease may occur in patients with ankylosing spondylitis. Pulmonary emphysema due to kyphosis and costovertebral joint involvement typically develops. Apical pulmonary fibrosis is the most common and characteristic feature of ankylosing spondylitis occurring in 3 – 4% of patients. Neurologic involvement is rare in ankylosing spondylitis. In some patients signs of peripheral nervous system involvement due to secondary thoracocervical or lumbosacral radiculitis are detected. In ankylosis and osteoporosis the spine is prone to fractures which can result in spinal injury. Atlantoaxial subluxation and displacement which may result in life- threatening spinal cord or brain stem compression may also occur. Chronic lumbosacral arachnoiditis (or epiduritis) occurs less commonly. It is often associated with sensitivity and motor disorders as well as dysfunction of pelvic organs. Cauda equina syndrome may also occur in patients with ankylosing spondylitis. Renal involvement occurs in 5 – 31% of patients with ankylosing spondylitis. Edema, hypertension, anemia and renal insufficiency usually occur at an advanced stage of the disease and are often associated with amyloidosis which is a very common complication of ankylosing spondylitis. Amyloidosis is typically caused by an active inflammatory process and highly progressive course of the disease. Immunoglobulin A (IgA) nephropathy has been also reported in association with ankylosing spondylitis. Urinary syndrome which is clinically manifested by proteinuria and microhematuria may be due to a prolonged administration of nonsteroidal anti-inflammatory drugs which often leads to drug-induced nephropathy. Gastrointestinal involvement. Asymptomatic inflammation of the colon and ileum has been observed in as many as 50% of patients with ankylosing spondylitis. However, 5 – 10% of patients with established ankylosing spondylitis develop Crohn disease or ulcerative colitis. Peculiarities of clinical as in males, females and children. In women exacerbations of the disease alternate with long-lasting remissions. Unilateral sacroiliac joint involvement is more common in females than in males. Women have aortic valve insufficiency more often than men. Men have more severe changes in the spine than women. However, women develop isolated ankylosis of the cervical part of the spine and distal joints of extremites more frequently than men. In children juvenile ankylosing spondylitis is typically revealed. Children have onset of symptoms before 16 years. The male-to-female ratio is similar to that of adults. It means that ankylosing spondylitis most frequently occurs in males than in females. Juvenile AS is characterised by peripheral arthritis of the joints of lower extremities, especially hip and knee joints as well as by enthesitis. Approximately 1/3 (one third) of children develop acute anterior uveitis. In the course of the disease they complain of pain in the back and sacroilial joints. Peripheral arthritis may disappear or persist. However, hip joint involvement is considered to be a poor prognostic indicator. Types of clinical course of the disease: 1. Slowly progressive course of the disease is characterised by spine and joint involvement occurring over years. The extent of the disease activity is usually low. 2. Slowly progressive course of the disease with exacerbations is characterised by alternation of remissions with exacerbations leading to disability of the patient. 3. Rapidly progressive course of the disease is characterised by pain syndrome, polyarthritis, muscle atrophy, weight loss, elevated indicators of active inflammation, rapid development of kyphosis and ankylosis. Septic type is characterised by an acute onset of the disease and is often associated with hectic fever, chills, excessive sweating, early signs of internal organ involvement. Septic type makes a definitive diagnosis of AS difficult. In this case ankylosing spondylitis must be differentiated from infectious endocarditis, sepsis and rheumatism. If fever and intoxication are followed by arthritis and stiffness in the spine, the diagnosis of ankylosing spondylitis can be made. Lab studies. No laboratory tests specific for AS exist. The ESR is elevated in 80% of patients and may not correlate with disease activity. Hypochromic anemia and leukocytosis are rare in ankylosing spondylitis. Other laboratory findings are slightly elevated, but in some patients they remain normal. In high disease activity the levels of circulating immune complexes and of immunoglobulins A, M and G in the blood serum are elevated. In peripheral arthritis non-specific inflammatory changes are typically revealed in the synovial fluid. They are the following: neutrophilic leukocytosis, elevated protein level, low viscosity. No ragocytes exist. The complement level is usually normal. Imaging Studies. In AS sacroiliitis is usually bilateral. Standard radiographs include frontal 25-30° projections in which the sacral bone does not overlap the iliac bone. The following X-ray stages of sacroileitis are typically singled out: 1) Initial or early stage. The first clinical manifestations of sacroiliitis are considered to be irregular margins of the bone forming the joint, foci of subchondral osteosclerosis and osteoporosis, pseudowidening of the articular space. 2) Stage of moderate injury. Irregular erosions of the margins of the joints, thinning-out of the articular space and pronounced subchondral sclerosis are typical of this stage. 3) Stage of pronounced injury. Periarticular sclerosis associated with formation of bone tissue in the foci of destruction and their partial ankylosis usually occur at this stage. Intervertebral spaces are typically narrowed and signs of ankylosis of true spine joints develop. 4) Late stage. Complete bone ankylosis and obliteration of joints, including sacroiliac, intervertebral and costovertebral with ossification of ligaments are typical of this stage. Sclerosis gradually decreases and leads to the radiographic appearance of osteoporosis at an advanced stage of the disease, and a compact thin line at the site of the sacroiliac joint (the so-called “pseudojoint”). Imaging studies of spine involvement. The most common and characteristic feature of ankylosing spondylitis is development of continuous (bridging) syndesmophytes between the adjacent vertebrae. They connect the edges of the upper and lower vertebral bodies. Syndesmophytes develop due to ossification of the peripheral part of intervertebral discs. Most commonly they appear at the junction of thoracic and lumbar vertebrae and are located at the lateral surface of the spine. Less commonly they occur on the anterior surface of the spine and very rarely – on the posterior surface. Over time, development of continuous syndesmophytes may result in a bamboo spine. At an advanced stage of the disease diffuse osteoporosis of vertebral bodies typically develops. Radiographic signs of anterior spondylitis should be also considered. Destructive changes of the upper and lower parts of the anterior surface of vertebrae typically lead to loss of the normal concave contour of the anterior surface of the vertebral bodies. Radiographic signs include squaring of the vertebral bodies. Intervertebral joint involvement associated with the development of ankylosis develop at an advanced stage of the disease. Lumbar part of the spine is usually the first to be involved. Thoracic part is the second to be involved and the cervical part of the spine is the third to be involved. These changes are better seen on oblique radiographs rather than on lateral ones. Sometimes ossification of ligaments of the spine is seen (especially of posterior longitudinal ligament and interosseous ligament). Changes of peripheral synovial joints. Standard radiographs usually reveal two types of changes. They are the following: 1) Ossification of the articular capsule, osteosclerosis, osteophytes, ankylosis of joints (most commonly – ankylosis of hip joints). 2) Erosive arthritis with involvement of foot joints, including metatarsophalangeal and interphalangeal joints, big toes. Enthesitis may develop radiographic changes, including foci of destruction at the sites of insertion of tendons on the spinal processes, crests of the iliac bone, ischial tuberosities, trochanters of femurs, knee-cap, clavicle and, especially on the calcaneus (for example, achillodynitis, plantar fasciitis). Diagnosis. Modified New-York criteria (1984) are widely used for diagnosing ankylosing spondylitis. They are the following:
  1. Low back pain with inflammatory characteristics
  2. Limitation of lumbar spine motion in sagittal and frontal planes
III. Decreased chest expansion IV.Radiographic signs of sacroileitis In patients suspected of having ankylosing spondylitis, obtaining radiographic signs of sacroiliitis and at least one of the three above-mentioned symptoms may help support the diagnosis. Determining HLA-B27 status is not a necessary part of the clinical evaluation. Moreover, determining HLA-B27 is not enough to make a diagnosis of ankylosing spondylitis. However, if no radiographic signs of sacroiliitis exist, determining HLA-B27 status may help support the diagnosis. Radiographic signs play a great role in making a diagnosis of ankylosing spondylitis. Computered tomography scan of the sacroiliac and spine joints with the use of radioactive technecium which accumulates in the foci of inflammation may reveal evidence of ankylosing spondylitis that is not apparent on standard radiographs. Differential diagnostics. Ankylosing spondylitis must be differentiated from other diseases associated with back pain and which occur more frequently than ankylosing spondylitis. AS must be differentiated from:
  1. Osteochondrosis of the spine
  2. Rheumatoid arthritis (especially in peripheral joint involvement)
III. Other seronegative spondylarthritis, including: 1) Psoriatic arthritis 2) Chronic reactive arthritis 3) Reuter syndrome 4) Arthritis in nonspecific ulcerative colitis (NUC) and Crohn’s disease 5) Whipple’s disease IV. Diffuse idiopathic skeletal hyperostosis V. Sacroileitis in brucellosis VI. Spinal tuberculosis Treatment. Treatment of ankylosing spondylitis should be complex, prolonged and regular. Kinesitherapy which includes an exercise program for maintaining spinal mobility and spinal joint unloading as well as deep-breathing exercises which promote chest expansion plays a major role in treatment of ankylosing spondylitis. It has been established that remedial exercises help improve spinal mobility and allow patients to work and perform usual activities. Most patients have to take anti-inflammatory drugs for pain relief. Pharmacologic treatment. Nonsteroidal anti-inflammatory drugs are usually used for long-term management. Full anti-inflammatory doses are typically used. The dose is usually reduced when the symptoms improve. Complete withdrawal of the drug is beneficial when pain is relieved. However, in an exacerbation of the disease nonsteroidal anti-inflammatory drugs should be renewed. Indomethacin is most commonly used in AS as it is thought to be the most effective NSAID for the treatment of AS. In severe spondylitis and pain syndrome the initial dose is usually 150 mg daily. As soon as the symptoms improve, the dose is reduced to 100 – 75 mg daily. Butadion is usually administered in the dose of 0,45 – 0,6 g daily. The maintenance dose is used when the symptoms improve. It is usually 0,3 – 0,2 g daily. Diclophenac may be as effective as indomethacin; however, it is better tolerated than indomethacin. The initial dose is 150 mg daily. It should be reduced to 100 – 75 mg daily when the symptoms improve. Cyclooxygenase-2 (COX-2) inhibitors, including meloxicam in the dose of 15 mg/day, celecoxib in the dose of 200 – 400 mg/day, nimesulid in the dose of 200 mg/day are also effective in reducing pain and inflammatory symptoms. Treatment of AS is aimed at reducing inflammatory symptoms. Sulfasalazine and Salazopiridazine are an effective treatment in AS without any systemic lesions. They should be administered in the dose of 2 – 3 g daily for 4 – 6 months. Then the maintenance dose (0, 5 – 1 g daily) is continuously used. They are beneficial in treating peripheral arthritis but ineffective in axial skeleton involvement. The use of D-penicillamin in treating ankylosing spondylitis has not been well studied. It is usually administered in the dose of 600 mg daily for 3 – 4 months. If the symptoms improve, the dose should be reduced to 150 – 300 mg/day. As complications such as Lyell’s syndrome, nephrotic syndrome, agranulocytosis may occur, it is necessary to make blood and urine analyses every 10 days during the first 3 months and later in life once a month. In severe progressive ankylosing spondylitis associated with fever and systemic manifestations treatment with cytostatics such as metotrexate in the dose of 7, 5 – 10 mg weekly, azathioprine in the dose of 100 – 150 mg daily, is necessary. Corticosteroids have a weaker effect in ankylosing spondylitis than in other inflammatory rheumatic diseases. In most cases corticosteroids are not beneficial in AS. Corticosteroids occasionally are helpful in treating extraarticular manifestations, including eye involvement (for example, iritis, iridocyclitis) and “septic” type of the disease. In this case high doses of prednisolone (30 – 40 mg daily) may be necessary. In peripheral arthritis local corticosteroid injections are useful. Vascular drugs such as pentoxiphillin, nicotinic acid (for 1 month 2 – 3 times a year) are typically used to improve microcirculation in affected joints, ligaments and muscles. Other medications are not used in the treatment of AS. Patients who develop severe muscle pains due to inhanced tone of perivertebral muscles myorelaxants, such as mydocalm in the dose of 100 – 150 mg daily and sirdalud in the dose of 4 – 6 mg daily, typically use. Non-pharmacologic treatment. Plasmapheresis and plasmosorption are usually undertaken to enhance the patient’s responsiveness to therapy in high immunologic activity in ankylosing spondylitis. 4 – 6 courses are usually enough. Remedial exercises are important to maintain spinal mobility and encourage an erect posture. The patient should perform special exercises which must not cause muscle straining several times a day. Such exercises turn out to be more effective and less painful after thermal procedures, including having a hot shower, applying healing mud or paraffin, etc., or application of dimethilsulfoxide. The patient should remember that it is necessary to maintain an erect posture during daily activities. The patients should master relaxing technique. Overloads and long-term bending (for example, riding a bicycle) should be avoided to prevent fractures of the spine. Swimming and walking are excellent activities to maintain mobility. Special attention should be paid to sleeping position of the patient. Sleeping on a firm mattress with a thin pillow tend to reduce the tendency towards flexion contractures; however in case of involvement of upper thoracic and cervical vertebrae, the patient should sleep without a pillow. Physiotherapy has a good effect in mild ankylosing spondylitis. Ultrasound with cortisone, inductothermia, electrophoresis with lidase, dimexide applied on the affected joints and spine, magnetotherapy and acupuncture are often used in treating AS. X-ray irradiation of the spine is used if the treatment is ineffective. Massage is recommended for strengthening back muscles. Hydrogen sulfide and radon baths may be also used. Orthopaedic measures are used very rarely. Splinting is used for prevention of contractures of peripheral joints, while bandages are used in rapidly progressive spine involvement with kyphosis. In severe contractures and ankylosis of peripheral joints, especially hip joints, surgery is used. Patients with severe arthritis of hip-joint usually need surgery. Hip replacement may be very useful to reduce pain and improve its function. In very rare cases, for example, in pronounced kyphosis, operations on the spine may be performed (cervical or lumbar osteotomy). In some patients these operations are successful and may help improve the condition, however, they entail great risk. Prevention. Primary prevention envisages education of people about genetic predisposition. Patients should be told about genetic predisposition of people to this disease, about the risk of developing AS in their children and necessity of a prolonged treatment. In case of revealance of a great amount of HLA-B27 carriers, primary prevention foresees elimination of infections, hardening, doing physical exercises aimed at postural training at the age of 12 – 14 years in boys. People belonging to high risk groups should be regularly checked for sacroileitis, iritis, iridocyclitis. Secondary prevention envisages prevention of exacerbations of the disease, adequate detection and treatment of extraarticular manifestations. The patient should be encouraged to give up smoking due to high risk of developing pulmonary involvement. Prognosis. Despite chronic progressive spondylitis most patients preserve work capability. Ankylosing spondylitis does not effect the patient’s life span. Mortality can occur related to spine injury and complications occurring after treatment such as gastrointestinal bleeding, aortic and respiratory insufficiency, amyloidosis. Hip joint involvement and ankylosis of all parts of the spine may lead to complete loss of work capability and ultimately, disability of patients.