, Juraj Payer2 and Manfred Herold3
(1)
National Institute for Rheumatic Diseases, Piestany, Slovakia
(2)
Fifth Department of Internal Medicine, Comenius University University Hospital, Bratislava, Slovakia
(3)
Department of Internal Medicine VI, Medical University of Innsbruck, Innsbruck, Austria
Ochronosis – see Alkaptonuria and Ochronosis, Arthropathy in ochronosis.
Oestrogens These female sexual steroids are more important to bone than the classical calciotropic molecules (PTH-1,25 (OH)2 vitamin D and somatotropin-IGF- I). The primary importance of oestrogens for bone integrity in both genders is likely to be associated with the early development of specific intracellular (cytosol) receptors during evolution.
The effect of oestrogens on bone and calcium homeostasis is complex. They have an inhibitory influence on the bone resorption – they protect against a proresorptive effect mediated by hormones and molecules (e.g. parathyroid hormone, thyroid hormones and heavy metals) and inhibit the release of cytokines from osteoblasts and peripheral monocytes. An effect on calcitonin and calcitriol regulation is exerted via specific oestrogen receptors on the osteocytes. The absence of oestrogens causes an overproduction of interleukin (IL)-1 by peripheral monocytes. Tumour necrosis factor (TNF)-α also increases bone resorption. IL-1 and TNF-α play a critical role in the pathogenesis of bone loss in the absence of oestrogens. Oestrogens also suppress the production of IL-6, which is induced by IL-1 and TNF-α. IL-6 is an important stimulator of osteoclast production. Oestrogen receptors are present on the surface of mononuclear cells, osteoblast precursors, osteoblasts and osteoclasts. At the same time, oestrogens stimulate the gene expression of the growth factor TGF-beta, which is an anabolic factor inhibiting the production of osteoclasts. Oestrogens also regulate the production of prostaglandins (PG) which influence the production and effectiveness of the cytokines. Except the aforementioned direct effect on bone, the absence of oestrogens leads to alterations of the calcium – phosphate metabolism. Oestrogen deficiency causes escalation of the osteoresorption; calcium excretion by the kidneys is decreased and calcium absorption in the gut via parathormone (PTH)-production of 1,25(OH)2 D3 is increased. The following rise of serum calcium causes a drop in PTH secretion and an increase in calcitonin secretion. This process leads to decreased osteoresorption, decreased intestinal absorption and increased calcium excretion. A decrease in serum calcium occurs, though within the physiological range. Oestrogen deficiency causes, via PTH effect, an increase of phosphate concentration in the blood. The decrease of PTH and increase of phosphates lead to a decrease in the production of 1,25(OH)2D3. All these adaptive mechanisms contribute to the deepening of the primary disturbance of the bone in oestrogen-deficient conditions. An early menarche, the number of pregnancies and hormonal contraception all have a protective influence against the occurrence of osteoporosis. As the pathophysiological overview shows, there is an acceleration of bone loss after the menopause. The yearly bone turnover in the premenopausal women affects approximately 2–5 % of cortical bone and 15–25 % of trabecular bone. Several recent studies stress the importance of oestrogen deficiency in the development of osteoporosis in men. The mechanism of the antiresorptive effect is identical to that seen in women.
Orencia Trade name of abatacept.
Orthoses Orthopaedic devices that help locomotive system function. They hold body parts in their correct position or move them into the correct position. Sometimes they compensate for lost function or correct a deficit to a manageable level.
Depending on their purpose, orthoses are divided into:
Therapeutic – can be used as temporary therapeutic or physiotherapeutic devices.
Compensatory – they permanently compensate a particular defect of the locomotive system, e.g. different length of limbs.
Prophylactic – used, for example, in sport to avoid unfavourable injury.
Static orthosis (stability)
Supportive – they compensate for loss of load capacity.
Fixative – they maintain stability where there is pathologic damage to the locomotive system; temporary (compensative) orthoses help, for example, during sequential therapy of fractures (plaster fixation), and permanent orthoses are used when the muscle system does not hold the joint in the required position as a consequence of a permanent defect.
Dynamic orthosis
Correct defective posture – e.g. corsets in the treatment of pathological curvature of the spine.
Movement control orthosis – e.g. orthosis used with knee instability where the orthosis prevents mediolateral movement, but anteroposterior movement can occur.
Orthosis influencing muscle work.
These are orthoses with dynamic functions. The function of weak muscles is taken over by the orthosis, which utilises:
The transfer of work from healthy muscle
Springs and rubber tension apparatus
The elasticity of material from which the orthoses are made
Hydraulic or electric drive
Orthosis of fingers.
Can be divided into fixative, redressive, retentive, substitute and movement regulating orthoses. A fixative or retentive orthosis is used in the rupture of the extensor pollicis longus muscle; the PIP (proximal interphalangeal) joint remains free. An extensive dynamic PIP orthosis enables the movement of the joint against resistance (flexion or extension). The three-point correction principle is used in boutonniere deformity (correction of flexion deformity in PIP and extension deformity in DIP – distal interphalangeal joint). In swan neck type deformity, the orthosis corrects extension deformity in the PIP joint and the flexion position in the MCP (metacarpophalangeal) and DIP joint.
A fixative thermoplastic splinter avoids ulnar or possibly radial deviation in the MCP joints. Spring extension splints of the fingers are used after orthopaedic hand operations in patients with hands affected by a rheumatologic process.
Orthopaedic shoes Suitable for individuals who owing to foot deformity (often in rheumatological diseases) cannot wear ordinary shoes. They are made for the purpose of foot deformity correction, pain relief and gait support, progression prevention and cosmetic cover for a deformed foot.
Orthopaedic shoe inserts Orthoses that are inserted into shoes in order to correct certain less serious foot defects. Correction inserts help actively or passively correct flattening of the arch of the foot. Relieving inserts contain holes for relieving the pain arising from sore areas (callosities). Correction inserts are used to correct different lengths of limbs.
OSCAR (osteoclast-associated receptor) A product of gene coding for the leucocyte receptor complex. It is specifically expressed in preosteoclasts and mature osteoclasts. OSCAR-L exprimed by osteoblast/stromal cells is its ligand. The presence of a soluble form of OSCAR in the co-culture of osteoblasts and bone marrow cells inhibits the formation of osteoclasts. OSCAR is therefore a specific regulator of osteoclastic differentiation.
Osgood–Schlatter disease Necrosis of tibial tuberosity of the femur in children, especially in 8–14-year-old boys. The defect is frequently bilateral. Patients complain of pain, particularly when climbing stairs. The pain is located in the area of the tibial tuberosity, which is swollen and tender to pressure. X-ray shows irregularity and calcification around the insertion of the patellar tendon.
► Treatment
Warmth and rest; a protective plaster is necessary in more serious cases. Improvement may take two or more years.
Osteitis deformans – see Paget’s disease.
Osteoarthritis (OA) A very common degenerative joint disease which progresses with age and characteristically affects the small joints of the hand, lower limb joints and the vertebral column. OA embraces heterogeneous diseases of different aetiological origins, but with a similar biological, pathological, radiological and clinical picture. It manifests itself by joint dysfunction due to dysregulation of cartilage metabolism, which leads to changes in the mechanical properties of cartilage. The pathological picture includes focal destruction of the cartilage as well as areas of remodelling in the form of osteosclerosis and osteophyte formation. OA can be primary or secondary (e.g. due to metabolic, endocrine, haematological diseases).
Risk factors of OA:
Heredity, particularly in the polyarticular form of small joints of the hands
Obesity, where it is associated with knee osteoarthritis
Hypermobility accompanying collagen abnormalities
Post-traumatic conditions
Sports with risk for joint injuries
Posture at work
► Clinical symptoms
Pain is typically associated with exercise and is associated with brief morning and inactivity stiffness. Gradually reduced function and immobility develop.
The X-ray picture shows loss of joint space and the development of sub-articular cysts, subchondral sclerosis, osteophyte formation and deformities. The course of OA is very variable and in most cases progresses very slowly. However, very rapid progression can occur.
Osteoarthritis – hands (Heberden and Bouchard type) A hereditary disease especially affecting women. The DIP (distal interphalangeal) joints are affected producing Heberden’s nodes whilst involvement of the PIP (proximal interphalangeal) joints cause Bouchard’s nodes. It commonly manifests itself between 40 and 60 years of age (menopausal).
► Clinical symptoms
Cartilaginous stiff nodes gradually grow on the opposite articular surfaces on the dorsal articular margins. The nodes are sore in the course of growth with intermittent inflammatory erythema and swelling. Deviation of the distal and middle phalanges is frequent. Once growth of the nodes stops, the affected joints become pain-free. Compared with rheumatoid arthritis, hand function usually remains good, though it may be a problem in certain jobs or pastimes (e.g. pianist). More often, it only causes cosmetic problems (knobbly-looking hands). Initially, the radiographs are normal, but later show unequal narrowing of the articular cavity and osteophyte formation. It is very important to emphasise to the patient that it is not rheumatoid arthritis or gout.
► Treatment
Non-steroidal anti-inflammatory drugs, or intra-articular glucocorticoids, are administered during inflammatory episodes. The use of SYSADOA is another option in more stubborn cases. Treatment may be supplemented by ultrasound administration, thermotherapy (wax, mud) and therapeutic exercise.
Osteoarthritis (OA) of the first carpometacarpal (CMC) joint (rhizarthrosis) OA may occur only in the first CMC (OA of the thumb) and the trapeziometacarpal joint. Rhizarthrosis is a common problem that affects mainly women in their 50s. The affection may be uni- or bilateral, with different clinical and radiological stages. As the cause is generally unknown, it is referred to as idiopathic. The most common symptom is pain, particularly in everyday movements at using the pinch function (touch the thumb with another finger) to turn keys, open a jar, a window and turn a knob. Little by little the joint deteriorates and later it subluxes. The result is then a characteristic deformation at the base of the thumb. Treatment is the same as in all other forms of OA, but if conservative treatment is insufficient, surgery may be indicated.
Osteoarthritis (OA) – pharmacological treatment
The pharmacological treatment of OA is represented by two large groups of drugs:
1.
SYRADOA (symptomatic rapid-acting drugs of osteoarthritis) can be simple analgesics such as paracetamol, aspirin, NSAIDs (non-steroidal anti-inflammatory drugs), opioids or intra-articular glucocorticoids.
2.
SYSADOA (symptomatic slow-acting drugs of osteoarthritis) such as intra-articular hyaluronate or oral glucosamine sulphate, chondroitin sulphate, diacerein, etc. (so-called chondroprotective agents).
Initially, simple analgesics usually provide satisfactory pain relief. In advanced disease, in order to suppress the inflammation and ease pain, NSAIDs are prescribed. Treatment with standard NSAIDs is associated with a number of adverse effects, particularly gastropathy (gastric ulcer, bleeding). The risk of gastrointestinal complications is increased in elderly patients who often suffer from OA.
In terms of these complications, NSAIDs with strong selectivity to cyclooxygenase 2 (COX-2) have a significantly lower incidence of adverse gastrointestinal effects. In terms of biological and biochemical properties, low-dose meloxicam belongs to this group. At the stage of painful OA, it is administered orally in a daily dose of 7.5 mg, but can be increased to 15 mg daily if required.
Another specific COX-2 inhibitor is celecoxib. Studies have shown that celecoxib is as effective as non-selective NSAIDs, when administered in a single daily dose of 100–200 mg. The safety profile of celecoxib has been extensively tested in comparative trial with diclofenac, ibuprofen and naproxen. These trials confirmed the favourable safety of celecoxib with less renal adverse effects and no increased cardiovascular risk.
Osteoarthritis – primary generalised nodal osteoarthritis (GNOA) Initially, it manifests by inflammatory episodes of the DIP (distal interphalangeal) and PIP (proximal interphalangeal) joints of the hand in relatively young women (around 40 years old), often perimenopausal. Familial incidence is frequent. It never affects the MCP (metacarpophalangeal) joints but often affects the knees, hips and intervertebral (facetal) joints. Initially, radiological changes are not visible, but typical osteoarthritic changes develop later. Deviation of the phalanges occurs.
► Treatment
Non-steroidal anti-inflammatory drugs are administered during inflammatory episodes. Afterwards, treatment is the same as in other forms of osteoarthrosis.
Osteoarthritis (OA): surgical treatment Surgical procedures play a key role in the treatment of OA. They are indicated when pharmacological and non-pharmacological treatment fails especially in severe hip and knee arthritis. The indications for surgical treatment include permanent severe pain (including night pain) and greatly reduced function of the affected joint with very limited mobility. At present, total hip or knee joint replacements are the most effective and frequently used procedure. Most patients are able to return to their normal daily activities after surgery. An improvement in the materials used in the development of the prostheses guarantees their longer durability up to 10–15 years.
Osteoblasts Uninuclear cells whose main function is the production of bone tissue (osteoformation). They develop from a pluripotent mesenchymal cell that gradually matures to preosteoblasts and osteoblasts. From a morphological point of view, they have a rounded nucleus localised in the basal part of the cell. In the nucleus, receptors for oestrogens, vitamin D3, integrins and cytokines can be found. The nucleus is localised on the opposite side to the position of contact between the osteoblast and the bone surface. The cytoplasm is heavily basophilic; the Golgi apparatus lies between the nucleus and the apical part of the cell. The endoplasmic reticulum is pronounced. The plasma membrane of active osteoblasts contains a high concentration of alkaline phosphatase and receptors for parathormone. Osteoblasts are localised on the surface of trabeculae and in the osteons of compact bone where they are capable of producing osteoid in the places of active osteoformation. After completion of the osteoformation phase, osteoblasts are transformed into lining cells or osteocytes.
Osteocalcin Primary non-collagenous protein of the bone matrix and dentin. It consists of 49 amino acids and its molecular weight is 58 kDa. It contains three residues of gamma-glutamic acid. It consists of osteoblasts and chondrocytes. Its production depends on the presence of K2 vitamin and is calcitriol-controlled. Osteocalcin provides a bond of the mineral component (calcium and hydroxyapatite) on the organic bone component. A part of newly produced osteocalcin is released into the circulation and reflects bone formation intensity. However, it is relatively labile and degraded by serum protease with fast decrease of in vitro immunoreactivity. Moreover, its rhythm is diurnal with peak values early in the morning. Nowadays, osteocalcin is regarded as better indicator of bone turnover than mere bone formation.
Osteochondritis dissecans – see König’s disease.
Osteoclasts Large multicellular cells containing 4–20 nuclei. The main function of osteoclasts is the resorption of mineralised bone matrix. Osteoclasts are formed by a fusion of unicellular phagocytic cells (monocytes) following development from preosteoclasts. There are receptors for calcitonin and integrin in their cytoplasm. Osteoclasts contain esterases and produce enzymes such as tartrate-resistant acid phosphatase, glucuronidase and carboanhydrase. They also possess colony-stimulating factor (CSF-1).
The nuclei of osteoclasts have no uniform appearance. There are numerous Golgi apparatuses, mitochondria and transport vesicles filled with lysosomal enzymes around the nuclei. Once activated, osteoclasts move to areas of microfracture by chemotaxis and come to lie in Howship’s lacuna and osteons of compact bone. The osteoclast resorption area is increased by a ruffled border from which it secretes hydrogen ions and several hydrolytic enzymes including cathepsin and matrix metalloprotease groups into the subosteoclastic space. As a consequence of the low pH, hydroxyapatite crystals dissolve allowing exposure of the bone matrix to the lytic enzymes and its resorption. Osteoclast activity is regulated by several hormones including parathormone, calcitonin and interleukin 6 (IL-6) and by osteoprotegerin and RANK ligand produced by osteoblasts.
Osteoclast-associated receptor – see Oscar (OsteoClastS-Associated Receptor).
Osteocytes These develop from osteoblasts and accumulate in the lacunae between the lamellae of compact bone and inside trabeculae. These cells were originally osteoblasts entrapped in the bone matrix that they produced and which was consequently calcified. The shape of osteocytes depends on their age and activity. A young osteocyte has many features in common with its precursor – the osteoblast – but is smaller with a smaller Golgi apparatus and endoplasmic reticulum. These changes are substantially more pronounced in older osteocytes with glycogen accumulation within the cytoplasm. Osteocytes possess cytoplasmic processes that form a net of cells in the bone channels. These processes facilitate the transport of cytokines, hormones, growth factors as well as signal transmission. Osteocytes work as sensors reacting to changes in the flow of fluids in bone channels. They react to these stimuli, induced by mechanical and environmental changes, by synthesis of active substances influencing the process of bone remodelling and by gentle adjustments of osteoblastic and osteoclastic activity. The other function of these stimuli is the nutrition of the bone tissue. During osteoclastic resorption of the bone, osteocytes undergo phagocytosis.
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