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Osteoarthritis Osteoarthritis is the most common type of joint disease. It is a degenerative disorder arising from the biochemical breakdown of articular (hyaline) cartilage in the synovial joints. It is characterized by loss of articular (the joint) cartilage as well as an abnormal growth of new bone (bone spur). Osteoarthritis involves not only the articular cartilage but also the entire joint organ, including the subchondral bone and synovium. Joints can be classified in functional or structural terms. Functional classifications, based on movement are synarthroses (immovable), amphiarthroses (slightly moveable) and diarthroses (freely A moveable). A structural classification categorizes joints as synovial, fibrous and cartilaginous. Normal synovial joints allow a significant amount of motion along their extremely smooth articular surface. These joints are composed of an articular cartilage, subchondral bone, synovial membrane, synovial fluid and joint capsule. The normal articular surface of synovial joints consists of articular cartilage (composed of chondrocytes) enclosed by an extracellular matrix that includes various macromolecules, most importantly proteoglycans and collagen. The cartilage enables joint function, protecting the underlying A subchondral bone by distributing large loads, maintaining low contact stresses, as well as reducing friction at the joint. Synovial fluid is formed through a serum ultrafiltration process by cells forming the synovial membrane (synoviocytes). Hyaluronic acid (HA, known also as hyaluronate) is also produced by the synovial cells, a glycosaminoglycan that is the major non‐cellular component of synovial fluid. Synovial fluid brings nutrients to the avascular articular cartilage, as well as providing the viscosity required to 1 absorb shock from slow movements, as well as the elasticity needed to absorb shock as a result of rapid movements. Pathophysiology This degenerative disease affects the whole joint, any joint can be affected. However, osteoarthritis most commonly affects the knees, hips, hands, neck and low back. It usually affects multiple joints but it can be isolated to one joint. It can lead to significant problems with mobility as well as having socioeconomic and psychosocial ramifications. There are a number of risk factors for osteoarthritis and these include increasing age, obesity, trauma, family history (genetics), decreased levels of sex hormones, myalgia, repetitive use, infection, crystal deposition, acromegaly, previous inflammatory arthritis, heritable metabolic causes, haemoglobinopathies, neuropathic disorders, disorders of bone, previous surgical procedures (e.g. meniscectomy). Pathologically in osteoarthritis, there are focal areas of damage to load‐bearing articular cartilage, new bone formation at the joint margins (osteophytosis), alteration in the subchondral bone (A sclerosis), inflammation of the synovium (synovitis) and thickening of the joint capsule. Osteoarthritis can be seen as a continuum of the normal repair process that occurs in all joint tissues as a result of joint trauma. In some people, however, it may be due to severe trauma or problems with the repair process; there is continued tissue damage with the result of symptomatic osteoarthritis. Conventionally, osteoarthritis was believed to affect primarily the articular cartilage of synovial joints; however, pathophysiological 2 evidence now demonstrates changes occurring in the synovial fluid, as well as in the underlying (subchondral) bone, the overlying joint capsule and other joint tissues. Osteoarthritis has been classified as a non‐inflammatory arthritis, yet increasing evidence demonstrates that inflammation occurs as cytokines and metalloproteinases are released into the joint. These agents are involved in the excessive matrix degradation that characterizes cartilage degeneration in osteoarthritis. In early osteoarthritis, swelling of the cartilage frequently occurs, reflecting an effort by the chondrocytes to repair cartilage damage. This may last for years or decades and is depicted by hypertrophic repair of the articular cartilage. As the condition develops, the levels of proteoglycans finally drop to very low levels, causing the cartilage to soften, with a loss of elasticity compromising joint surface integrity further. Microscopically, flaking and fibrillations (vertical clefts) develop along the usually smooth articular cartilage on the surface of an osteoarthritic joint. Loss of cartilage results in loss of joint space as time progresses. Erosion of damaged cartilage in an osteoarthritic joint progresses until there is exposure of underlying cartilage and the protective cartilage continues to articulate with the opposing surface. The damaged subchondral bone can also undergo cystic degeneration. Osteoarthritic cysts are also referred to as subchondral cysts, pseudocysts, or geodes. Fragmentation of these osteophytes or of the articular cartilage itself results in the presence of intraarticular loose bodies. 3 Signs and symptoms The progression of osteoarthritis is typically slow, occurring over several years or decades. The patient can become less and less active, and more susceptible to morbidities related to decreasing physical activity. Structural changes can often occur, with no accompanying symptoms, but joints may appear normal. Pain is often the first source of morbidity, described as being deep, achy joint pain exacerbated by extensive use; there may be a reduced range of movement and crepitus. Stiffness during rest can develop, along with morning joint stiffness. In the beginning pain can be relieved by rest and responds to simple analgesia. Pain may become more evident even during rest and not respond to medications. There may be joint swelling/synovitis, periarticular tenderness, bony swelling and deformity, and muscle weakness/wasting around the affected joint. Investigations Diagnosis is typically based on clinical examination. When disease is advanced it can be seen on plain X‐rays. MRI may be useful to distinguish other causes of joint pain. For swollen joints joint aspiration may be considered. Management The goals of treatment include alleviation of pain and improvement of functional status. Patients should receive a combination of non‐pharmacological and pharmacological treatment. National guidelines are available. 4 Osteoporosis Osteoporosis is a chronic, progressive disease of multifactorial aetiology. The condition is a systemic skeletal disease depicted by low bone mass and micro‐architectural deterioration of bone tissue; this then leads to an increase in bone fragility. It is not until a fracture occurs that the disease becomes clinically apparent. Many people experience pain, disability and diminished quality of life as a result of having this condition. Because this condition is so often clinically silent before manifesting in the form of fracture, the adverse effects of osteoporosis are in part often overlooked and undertreated. Failing to identify those people at risk, to educate them and to put in place preventive measures can lead to tragic consequences. Although it is a preventable disease, osteoporosis can result in devastating physical, psychosocial and economic consequences. Prevention and recognition of the secondary causes of osteoporosis are first‐line measures to lessen the impact of the condition. The World Health Organization’s definition of osteoporosis is based on bone mineral density (BMD) measurements in white women. The definition applies to post‐menopausal women and men aged 50 years or older. Initially bone formation exceeds bone resorption, but by the time the person reaches 30 years of age this has reversed, resulting in a net loss of bone mass, leading to increased bone fragility and susceptibility to fracture. 5 Osteoporotic (fragility) fractures result from mechanical forces that would not normally result in fracture. Osteoporotic fractures are defined as fractures associated with low BMD; they include spine, wrist, hip and shoulder fractures. Pathophysiology There are multiple pathological factors that interact in the development of osteoporosis, some are discussed here. There is an imbalance in remodelling in osteoporosis, with a relative increase in resorption that has not been matched to the related increase in bone formation. The bone matrix is mineralized as is usual but there is less bone. Bone remodelling is controlled by a number of cytokines, including interleukins, colony stimulating factors and calcitrophic hormones, such as parathyroid hormone (PTH), 1,25‐dihydroxyvitamin D, calcitonin and oestrogen. This imbalance in bone remodelling causes lower bone density and bone quality, resulting in bone fracture. Whilst age is a factor in the development of osteoporosis, other circumstances are also indicated, for example when there is reduced mechanical loading as occurs when a person is immobilized or confined to bed rest, the menopause (when there is a reduction in sex hormone concentration) and if there is an excess of corticosteroids. Common sites of fracture after minor trauma, due to osteoporosis, include the spine, wrist, hip or pelvis; however, any bone can be affected. There are several risk factors associated with osteoporosis (see 6 Table 55.1). Oestrogen deficiency accelerates bone loss postmenopausal women and plays a role in bone loss in men. This can lead to excessive bone resorption, accompanied by inadequate bone formation. Osteoblasts, osteocytes and osteoclasts all express oestrogen receptors. In addition, oestrogen affects bones indirectly through cytokines and local growth factors. An oestrogen‐replete state may enhance osteoclast apoptosis via increased production of transforming growth factor beta. Bone loss that accompanies ageing, in contrast to post‐�آ menopausal bone loss, which is associated with excessive osteoclast activity, is associated with a progressive decline in the amount of osteoblasts in proportion to the demand. This demand is determined by the frequency with which new multicellular units are created and new cycles of remodeling are commenced. Calcium, vitamin D and PTH assist in the maintenance of bone homeostasis. Inadequate dietary calcium or reduced intestinal absorption of calcium caused by ageing or disease may lead to secondary hyperparathyroidism. PTH is secreted in response to low serum calcium levels, increasing calcium resorption from bone, decreasing renal calcium excretion and increasing renal production of 1,25‐dihydroxyvitamin D that enhances calcium and phosphorus absorption, and inhibits PTH synthesis and bone resorption. Vitamin D deficiency can result in secondary hyperparathyroidism via decreased intestinal calcium absorption. 7 in Signs and symptoms The process that leads to established osteoporosis is asymptomatic as the condition typically presents only after fracture. The clinician should remember that osteoporosis occurs in many people who have no symptoms, or just a few risk factors. Investigations Diagnosis of osteoporosis centres on the assessment of BMD using dual‐energy X‐ray absorptiometry (DEXA). The following screening blood tests should be considered, in those people with osteoporosis, to identify treatable underlying causes: full blood count, urea and electrolytes, liver and thyroid function tests, serum calcium, alkaline phosphatase, serum immunoglobulins and paraproteins, urinary Bence‐Jones’ proteins. In men testosterone/gonadotrophins should be screened. Treatment is aimed at fracture prevention and includes modification of general lifestyle factors, such as increasing weightbearing and muscle‐strengthening exercise and ensuring optimum calcium and vitamin D intake as an adjunct to active anti‐fracture therapy. Currently, no treatment can completely reverse established osteoporosis. Pharmacological measures include the administration of adequate calcium, vitamin D and anti‐osteoporotic medication such as bisphosphonates, PTH, raloxifene and oestrogen. In addition, potentially treatable underlying causes of osteoporosis such as hyperparathyroidism and hyperthyroidism should be ruled out or treated if detected. Surgical care includes vertebroplasty and kyphoplasty; these are 8 minimally invasive spine procedures used for the management of painful osteoporotic vertebral compression fractures. The first goal is to control pain if a fracture has occurred. Oral analgesics on a regular basis can be implemented. Moist hot packs and transcutaneous electrical nerve stimulation should also be considered. A comfortable mechanical support for the spine and in some cases, a thoracic orthosis may need to be prescribed (this helps to limit motion in the spine); hip protectors can also be used. 9