Sacroiliac block (SI block) Sacroiliac pain is a frequent reason for vertebrogenic pain syndrome. SI block is blockade of one or both SI joints. Symptoms can be confirmed as arising from the sacroiliac joint by various methods, e.g. hyperabduction phenomenon according to Patrick, by springing the SI joints in the prone and supine positions and by tenderness over the affected SI joint in the standing position.

Sanfilippo’s disease – see Mucopolysaccharidosis (MPS).

The clinical picture is characterised by pain and oedema in the sternal area. The disease leads to limited movement of the arms and shoulders. Pain localised to the acromioclavicular joints may also be present. Osteolytic lesions in the sternum and rarely in the mandible may develop later on in the course of the disease. Less frequently, ossification of the ribs, sternum and sternoclavicular joint occurs. Focuses of sterile osteomyelitis are present in the histopathological picture. The aetiology of the disease is unknown, though in a few cases disseminated infections due to Propionibacterium acne were reported. Treatment is non-specific; antibiotics are not effective. Nonsteroidal anti-inflammatory drugs, sulfasalazine and methotrexate have benefited certain patients. Recent studies have shown significant improvement after intramuscular administration of calcitonin or intravenous pamidronate. The differential diagnosis includes ankylosing spondylitis, psoriatic arthritis, fibromyalgia, bacterial infections and relapsing polychondritis.

SARA – see Sexually acquired reactive arthritis (SARA).

Sarcoidosis – see Musculoskeletal manifestations of sarcoidosis.

SARD Sometimes used abbreviation for systemic autoimmune rheumatic diseases which include autoantibody associated rheumatic diseases (AARD) as well as chronic inflammatory rheumatic diseases like rheumatoid arthritis (RA), juvenile idiopathic arthritis (JIA) and others.

Sausage toe – see Toe swelling/deformity and associated diseases.

Scheie’s disease – see Mucopolysaccharidosis (MPS).

Scheuermann’s disease Juvenile kyphosis and idiopathic scoliosis are severe disorders of a growing vertebral column. Hereditary, hormonal, nutritional factors, blood supply impairment and mechanical overloading cause osteochondrosis of vertebral end plates and herniation of the nucleus pulposus into vertebral bodies called Schmorl’s nodes (Christian Georg Schmorl, German pathologist, 1961–1932). The condition leads to wedging deformities of vertebrae, narrowing of intervertebral discs and kyphosis of the thoracic spine compensated by significant cervical and lumbar lordosis.

Schmid’s dysplasia An autosomal dominant hereditary metaphyseal dysplasia associated with mild short-limbed dwarfism without shortening of the vertebral column. Epiphyses of long bones are denticulate; metaphyses are deformed in caliculus shape. Affected individuals suffer from genu varum and coxa vara. Schmid’s dysplasia becomes obvious after the third year of life; initially the dysplasia may suggest rickets but serum levels of calcium, phosphate and alkaline phosphatase are within the normal childhood range.

Schmorl’s nodes – see Scheuermann’s disease.

Schober’s test – see Metric measurement of vertebral column in spondyloarthritis (SpA).

Schober’s test modified – see Metric measurement of vertebral column in spondyloarthritis (SpA).

SCID – see Severe combined immunodeficiency (SCID).

SCID mice (Severe combined immunodeficiency mice) A species of mice with serious genetic combined immunodeficiency (SCID) which causes them not to develop antibody or T-cell immunity and so allow them to serve as ‘live test tubes’ for implanting lymphocytes from other animal species. When, for example, human lymphocytes are injected, they can produce antibodies of human isotypes after antigen stimulation. The nature of the primary disorder is a mutation on chromosome 16 causing deficient activity of an enzyme involved in DNA repair, leading to failure of haematopoietic stem cells of the lymphoid line to mature.

Sclerosteosis A progressive autosomal recessive disorder characterised by an excess of bone stock due to insufficient expression of the SOST gene. It shows radiologically as a generalised hyperostosis and sclerosis leading to a markedly thickened and sclerotic skull, mandible, ribs, clavicles and all long bones. Sclerostin is a protein product of the SOST gene competing with bone morphogenic products (BMPs) for receptor types I and II of these proteins on osteoblasts. Sclerostin decreases the signalling induced by BMPs and suppresses the osteoblast-induced mineralisation. The expression of SOST has been detected in osteoblast cultures and in sites of mineralisation of the skeleton. A strong expression in osteocytes indicates that through these cells sclerostin modulates bone homeostasis. Transgenic mice with increased expression of SOST have low bone stock and decreased firmness of the bones.

Sclerostin A glycoprotein produced by osteocytes and some chondrocytes. It belongs to the group of bone morphogenetic protein (BMP) antagonists. It binds to LRP5/6 receptors and attenuates the Wnt signal cascade. This results in suppression of bone formation. The production of sclerostin is reduced by mechanical load, parathyroid hormone and prostaglandin E2 and increased by calcitonin. Inactive mutation of gene encoding sclerostin (SOST) results in diseases characterised by hyperostosis (sclerostosis, van Buchem). Since sclerostin is bone tissue specific, preparations for the treatment of osteoporosis based on antibodies against sclerostin are being developed. They are already in human trial stage and their release to the market is estimated in 2017.

Scoliosis The curvature of the vertebral column in the frontal plain. Scoliosis is considered to be the lateral curvature of the vertebral column in a range greater than 11˚. Scoliosis can be functional (the curves are not fixed and can be corrected actively or passively) or structural (the curves are fixed).

Scurvy – see Musculoskeletal symptoms in scurvy.

Secondary gout A condition in which gout is caused by hyperuricaemia secondary to overproduction of uric acid from increased cellular turnover or decreased excretion of uric acid by renal disease or effects of drugs. Lymphoproliferative and myeloproliferative diseases, certain malignancies (usually carcinomas in disseminated malignancies and more frequently in anaplastic malignancies) and haemolytic anaemia belong to those conditions that are associated with overproduction of uric acid. Chronic renal insufficiency, chronic lead poisoning, drugs (diuretics, low-dose salicylates, pyrazinamide, nicotinic acid and ethambutol) and also endocrinopathies (hyperparathyroidism, hypothyroidism) are amongst conditions associated with decreased renal elimination of uric acid.

Secondary hyperparathyroidism The increased concentration of parathormone is in response to calcium deficiency with the most frequent cause being a vitamin D deficiency. Treatment of the underlying cause is the treatment of choice.

Secondary osteoporosis Develops as a result of another primary disorder or as a consequence of treatment. In spite of its low prevalence, approximately 10 %, it is important to rule it out as a cause of osteoporosis. Exclusion of secondary osteoporosis is often demanding especially in patients in whom it is suspected on the basis of the medical history, clinical examination and laboratory findings, as well as in patients in whom the bone mineral density measured for age is low or the elapsed time since the menopause. In men, a thorough differential diagnosis is imperative as several authors report its occurrence in more than 70 % of cases. The importance of distinguishing secondary osteoporosis often lies in a diametrically different therapeutic approach. The most frequent causes of the secondary osteoporosis include disorders of the gastrointestinal tract, pancreas, liver and kidneys, endocrine and rheumatic diseases and drug-induced osteoporosis.

Selectins A family of glycoprotein leukoadhesive molecules which consist of three members: L-selectin (CD62L, previously referred to as MEL-14), P-selectin (CD62P, previously referred to as PADGEM) and E-selectin (CD62E, previously referred to as ELAM-1). The nomenclature is derived from the cell types, which possess particular selectins on their surface: L-selectin on leucocytes, P-selectin on platelets and after induction by cytokines on endothelial cells and E-selectin on endothelial cells. The molecules of selectin have the lectin domain on the N-terminal of the molecule through which they can bind to the specific ligand. These are saccharides in adhesive molecules similar to mucin. This is the fundamental of their biological function as such lectin–saccharide interactions (lectins) are particularly involved in the binding of leucocytes to the vascular endothelium and subsequently in their migration from postcapillary venules to the tissue affected by inflammation.

Selective oestrogen receptor modulators (SERM) At present, raloxifene is the only member on the market licensed for the treatment of osteoporosis. It acts on bone as an oestradiol agonist, producing a decrease resorption and an increased proliferation of osteoblasts. As an oestradiol agonist, it influences the cardiovascular system (even though in contrast to oestradiol, it does not increase the total HDL and CRP). Raloxifene is an oestrogen antagonist of receptors in the endometrium and breasts. It significantly reduces the risk of vertebral and nonvertebral fractures in women with severe osteoporosis, and a reduced risk of invasive breast cancer (84 %) is considered an additive and very important effect. A possible positive influence on cardiovascular events is promising. Raloxifene is also effective in the prevention of osteoporosis. An increased risk of venous thromboembolism with raloxifene is comparable to oestrogens and hot flushes may also be accentuated. Therefore, it is not suitable for patients with a history (or family history) venous thromboembolism and for women with climacteric problems.

Semiquantitative assessment of vertebral deformities The assessment of changes in the height of vertebral bodies in the lateral projection has a great significance, especially in predicting further fractures, in patients with osteoporosis. A semiquantitative assessment, according to Genant, is the most frequently used method in clinical practice. A decrease of anterior height of a vertebra by 20–25 % is assessed as 1st degree or mild fracture, with a decreased height by 25–40 % as 2nd degree or moderate vertebral fracture and a decrease by 40 % and more as 3rd degree or severe fracture.

Senile arm In some cases, a careless movement of the arm can cause bleeding to the joint cavity, so-called Milwaukee arm, which presents serious complications for further treatment.

Senile shoulder Chronic shoulder pain with polytopic symptomatology. The pain is caused by degenerative changes of periarticular soft tissue in old age. Tendon ruptures and atrophy of the rotator cuff are often present.

Senile osteoporosis (type II) A mild-degree atrophy of the bones is a physiological phenomenon and belongs to the normal involution of ageing. A pathological state occurs when bone loss is excessively enhanced and the bone mineral density level decreases below the osteoporosis limit defined in the individual age groups of men and women on the basis of WHO criteria – see the entry diagnostics of osteoporosis.

SERM – see Selective oestrogen receptor modulators (SERM).

Serum amyloid A (SAA) A family of polymorphous proteins encoded by various genes on chromosome 11 in a number of mammal species. There are two human acute phase SAA proteins (SAA1 and SAA2), with 5 isoforms of SAA1 and 2 isoforms of SAA2. The physiological concentration of SAA in serum is approximately 2–3 mg/l but can increase by 1000 times in acute inflammation (similarly to C-reactive proteins). In terms of function, SAA are small lipoproteins, which during the acute phase of inflammation join the third fraction of high-density lipoproteins (HDL3) and become a dominant apolipoprotein in such molecules. SAA inhibits thrombin-induced activation of platelets as well as the activation of neutrophils to prevent oxidative tissue destruction during the course of inflammation. SAA is beneficial in acute inflammation but is harmful in chronic inflammation (causing amyloidosis).

Severe combined immunodeficiency (SCID) This is a heterogeneous group of disorders caused by defects in the development of stem cells of the lymphoid line with the subsequent occurrence of serious disturbances in T- and B-lymphocyte functions. It is one of the most severe immunodeficiencies as there is almost complete absence of humoural and cellular immunities. Children with SCID have very severe lymphopenia (decreased peripheral lymphocyte count) with blood lymphocytes being functionally inactive. A severe agammaglobulinaemia develops within the first months of life. The thymus is either missing or present only in remnants localised in untraditional anatomic sites. There are also numerous disturbances observed in phagocytosis. Severe recurrent infections, including pneumonias, chronic otitis media, chronic diarrhoea and sepsis begin soon after birth. The body rapidly becomes overwhelmed by recurrent infections and children with SCID usually do not live to see the second year of life. The development of infection can only be prevented by a sterile birth and complete isolation of the child in a sterile environment for its whole life. SCID has several forms depending to the type of cells affected and the molecular defects, especially in the activity of various enzymes. Treatment is possible via bone marrow transplantation or gene therapy (supplementing missing or defective genes).

Sexually acquired reactive arthritis (SARA) Reactive arthritis secondary to sexually acquired infection with chlamydia being the most frequent pathogen.

Sharp score – see Total Sharp score.

Shock A systemic reaction of the body to sudden and intensive nonphysiological impulses from the external or internal environment. It is manifested particularly by hypotension and respiratory distress. Depending on the underlying cause, the shock can be subdivided into traumatic, haemorrhagic, cardiogenic, anaphylactic or endotoxic (septic) shock. Reduced tissue perfusion and insufficient oxygen delivery were considered as the typical cause. Lately, impaired mitochondrial function (defect of oxidative phosphorylation) has been included. At present, defects of certain mitochondrial enzymes, increased synthesis of nitric oxide and reactive oxygen intermediates, increased adhesion of neutrophils on endothelium and activation of pro-inflammatory cytokines are considered the main causes of hypotension. The condition of shock is thus the result of an imbalance between NO, superoxide and their metabolites.

Shoulder–hand syndrome – see Algodystrophic syndrome (ADS).

Shulman’s syndrome – see Eosinophilic fasciitis (Shulman’s Syndrome).

Sickness impact profile (SIP) – see Instruments of assessing (health status measurements, outcome measurement).

Signals of functional impairment (SOFI) – see Instruments of assessing (health status measurements, outcome measurement).

Silicone synovitis Develops as a reaction to a foreign body or to certain components of silicone arthroplasties (silicone elastomer, dimethylpolysiloxane). Clinical symptoms include pain, stiffness and swelling of the joint with implanted silicone prosthesis. Silicone synovitis most frequently affects carpal and metacarpal implants and radial prostheses.

Sine syndromes Sine syndromes (SSs) represent a problem in clinical medicine, especially if the diagnosis is not determined by pathognomic findings, e.g. identification of microbial pathogens, sodium monouratic crystals, etc. SSs are topical especially in diseases defined by diagnostic and/or classification criteria, whilst in SSs a criterion with nomenclature meaning can also be missed. Early recognition of an SS variant of a considered diagnosis is as urgent as in its completely manifested form, because the prognosis and requirements for the early initiation of efficient therapy are identical. SSs require individual approaches and implementation of the principles of personalised medicine in everyday clinical practice. A patient with an SS has the right to expect the same quality of health care as a patient with a standard manifestation of the same disease. The capability of recognising an SS does not mean only a challenge for the attending physician but also a feedback test of his/her expert knowledge.

Sine syndromes in ankylosing spondylitis The diagnosis of ankylosing spondylitis is based on the proof of sacroiliitis on X-rays. Therefore, the term of ‘ankylosing spondylitis without sacroiliitis’ might seem illogical. However, clinical course of ankylosing spondylitis is highly variable, ranging from mild asymptomatic forms to rapidly progressive ones resulting in spine ankylosis, replacement of hip joints in rhizomelic forms or even in extra-articular manifestations. Thus ankylosing spondylitis can be well “hidden” in this broad spectrum of clinical manifestations. New conception of axial (and peripheral) spondyloarthritis throws some other light to these issues, which can explain these forms as so-called pre-radiographic stage of axial spondyloarthritis.

Sine syndrome in articular chondrocalcinosis Chondrocalcinosis is caused by abnormal deposition of calcium pyrophosphate dihydrate crystals into cartilages. Release of the crystals into synovial space results in episodes of arthritis and secondary osteoarthritic changes. Chondrocalcinosis does not have a characteristic clinical presentation but typical radiological finding of calcifications in articular cartilages and ligaments. Pathognomonic is the proof of calcium pyrophosphate dihydrate crystals with positive double refraction in polarised light.