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Low Bone Density in Old People - Coursework Example

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This coursework "Low Bone Density in Old People" presents bone tissue formation and development that is facilitated by the activity of osteoblast and osteoclast cells, and usually, this is achieved through calcium and phosphorus deposition and resorption from the bone respectively…
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OSTEOPOROSIS (LOW BONE DENSITY) IN OLD PEOPLE OSTEOPOROSIS IN AGED PEOPLE 25th August, 2012 Table of Contents Abstract Introduction Risk and predisposing factors Osteoporosis and Osteopaenia in old people Aetiology Clinicals signs Therapeutic management and Prevention Discussion Conlusion References Abstract Bone tissue formation and development is faccilitated by the activity of osteoblast and osteoclast cells, and usually this is achieved through calcium and phosphorus deposition and resorption from the bone respectively. At around the age of 35 years there is an increased activity of osteoblasts for bone tissue deposition but later in old ages the activity of osteoclasts in bone resorption. Osteoporosis is a bone disease characterised by low mineral mass in the bone leading to fragility and risk for fracture. A great part of the reduction in bone mineral density (BMD) observed in older people has been attributed to disuse of the skeletal system rather than the aging process itself (Lewielki, 2004). While some mechanical stress is needed to maintain optimal bone mineral density, it is not clear which types of exercises are most valuable for better skeletal system development or whether appropriate exercise might reduce the need for estrogen therapy in postmenopausal women. Cross-sectional studies indicates that physical activity, aerobic fitness, and strength have all been correlated with establishment of a proper bone mineral density, and therefore a strong musculoskeletal system. Young people who use a specific part of the body in vigorous exercise exhibit enhanced bone density in that part of the body, but not necessarily in other regions, although older people who have been active for many years seem to exhibit generally enhanced bone mineral density. Prospective studies have shown that most regimens used for vigorous aerobic and strength training enhanced bone mineral density, but walking is relatively ineffective for prevention of postmenopausal bone mineral loss (Maclean et Al., 2008). Introduction Osteoporosis is a musculoskeletal system disease which affects the bone tissue rendering them brittle and prone to fracture in other words, the bone looses its mineral density. Osteoporosis is diagnosed when bone density has decreased to the point where fractures occur with mild stress. Osteoporosis, or porous bone, is a disease characterized by low bone mass and structural deterioration of bone tissue, leading to bone fragility and an increased risk of fractures of the hip, spine, and wrist. The elderly people in our society are usually at risk or affected by osteoporosis, a disease that can be prevented and managed therapeutically (Greenspan, 2007). Osteoporosis is a major health problem in the general population facing the society's older generation in an even distribution along all sexes. Adults until they reach around the age 40, the process of breaking down and building up bone mineral tissue by osteoclasts and osteoblasts cells continues in a nearly perfectly coupled system, and the two phases balance each other. As a person's age go beyond 40 or in the presence of certain conditions, this balanced homeostatic system of bone formation breaks down and the two processes become out of synchronization leading to bone tissue weary. The reasons why this risk to osteoporosis occurs during aging have not been studied, but declining levels of sex hormone and hormonal imbalance may be one of the attributes. Eventually individual body homeostasis leads to breakdown mechanism overtaking the buildi-up mechanism leading to osteopaenia and exposure to osteoporosis. Women are under high risks of development of this disease and for instance about eighty percent osteoporosis occurs in women and 20% in men. The large proportion of diseased women occurs most commonly at the age of post-menopause, and this has been related to the deficiency of estrogens (Marshall et Al., 1996). Clinically the affected patients demonistrates signs of back pain, loss of height and stooped posture before the actual fracture occurs. Risk and Predisposing Factors for Osteoporosis Risk factors include fracture during falling in addition to low bone mineral density, falling is the primary risk factor for fractures. This disease can also be associated with the aged's chronic medical problems such as emphysema, heart disease, stroke, arthritis, and depression, with the risk increasing with multiple health problems. Taking multiple medications especially tranquilizers and antidepressants poor physical function, importantly slow gait and reduced muscle strength. Inactivity that results in weak thigh muscles and poor balance particularly puts any older person at risk for fracture and particularly those with low bone density. A lot of risk factors have been associated with the development of osteoporosis and the contribution to an individual’s likelihood of developing the disease. These includes; gender, age, hormonal changes, mineral intake especially calcium and phosphorous, genetic and body size, but generally women are highly exposed to developing osteoporosis as compared to their male counterparts due to less bone tissue proportion to the muscle cover as well as changes of menopause (Siris et Al., 2001). The ageing population show greater risk of developing osteoporosis, since with age the activity of osteoclast cells increases rendering bones thinner and weaker. Persons with a small body and thin-bonned size may be at an high risk as compared to large body sized individuals especially in the women. Also there is a genetic predisposition to development of thos disease, and usually African Americans and Hispaniards are at low risk as compared to Asians counterparts. Hormonal imbalances as seen in the absence of menstrual periods (amenorrhea), low estrogen level (during menopause), and low testosterone (T4) levels in men can act as a predisposing factor to osteoporosis. Conditions such as anorexia nervosa which can be characterized by an irrational fear for weight gain, and this eating disorder increases risk for osteoporosis (Benito M., 2005). Low calcium intake as well as vitamin D in the diets may be another predisposing factor for loss of bone mineral density. Also a long period exposure to certain medications such as glucocorticoids and some anticonvulsants can result into loss of bone density and fracture risks. Some lifestyle which allows for body exercise inactivity may result into the weakening of the bone tissue strength and thus expose these individuals to osteoporosis. Too much cigarette smoking and alcohol consumption predispose individuals to exposure to bone loss and subsequently fractures. Osteoporosis and Osteopaenia in old people Aetiologay The causal agents for the development of osteoporosis as a skeletal disease condition lies in a composite of pathoological factors which includes; poor mineral intake such as phosphorous and calcium, lack of proper exposure to exercise as well as hormonal imbalance especially for the women (Khosla, 2010). Clinical symptoms Histologically this disease condition is defined as bone disease characterized by low bone mineral mass and microarchitectural deterioration of bone tissue resulting to bone fragility and increased susceptibility to fractures under falling. Clinically the most frequently sites of bone fracture are hip, spine and wrist, hence these osteoporotic fractures have a considerable economic impact due to levels of mortality, morbidity and medical costs. Osteoporosis is a preventable and treatable disease, especially if diagnosed early. The preferable method of diagnosis is measurement of Bone Mineral Density (BMD). Low bone mineral density is the single best predictor of the occurence of fracture especially as seen in the asymptomatic postmenopausal women. This can be determined by T-Score evaluation and therefore this can be used to determine the BMD level and the presence or risk of osteoporosis (Khan and Syed, 2004). A T- Score is the standard deviation variance of patient's BMD compared to a standard healthy young individual reference in a given population. According to WHO, individuals with a T-Score below -2.5 have osteoporosis and those with a T-Score between -1 and -2.5 have a low bone density and are at risk for fractures and are thought to be involved with Osteoporosis as well as Osteopaenia. Bone has a similar degree of the breakdown and growth balance to allow for the organ to undergo its establishment through bone tissue resorption and deposition. This results to proper remodelling and this can also be seen in other organs of the body, as there is an homeostatic balance through bone tissue is constantly being broken down and reformed again. This turnover is necessary especially for growth, for repair of minor damage that occurs from frequent stress, and also for the maintenance of a properly functioning body skeletal system. This is achievable by the function of two essential cells involved in this process, which are osteoblasts and osteoclasts. Osteoclast cells which are formed from certain blood cells and are responsible for the mineral breakdown, or resorption, of the bone tissue from the skeleton. These cells develop holes into the bone in the event of releasing the small amounts of calcium into the blood circulation that are necessary for other vital functions of the body. However the osteoblast cells are produced by bone stem cells and are the bone tissue deposition as well as formation. They rebuild the skeleton by forming the bone tissue, first by filling in the holes with collagen, followed by laying down of crystals of calcium and phosphorus. The balance of bone build-up (formation by the osteoblast cells) and break down (resorption by osteoclast cells) is controlled by a complex mix of hormones and chemical factors. Usually when bone resorption occurs at a greater rate than bone build up, there is an ultimate loss of bone mineral density and this puts an individual at risk for osteoporosis. Also in women, estrogen loss after menopause is associated with hormonal imbalance that can be associated with a rapid resorption and loss of bone density (Riggis and Melton, 1995). This then results in the predisposing factor for these group of people to be exposed to highest risk for osteoporosis disease development and therefore for fracture risks. Prevention The most essential way of prevention of bone mineral through osteopaenia or osteoporosis loss is exposure to appropriate exercises. Most studies using specific bone-loading exercise have shown substantial increases in bone density at the specific sites loaded, but elderly people seem incapable of responding favorably to vigorous exercise. Studies have not indicated a direct relationship between exercise and estrogen therapy. Extremely high volumes of vigorous exercise may overwhelm a person's adaptive capacity especially the aged, leading to stress fractures. For instance, young women athletes may be at a risk of suffering from menstrual dysfunction exhibit reduced bone mineral density and musculoskeletal disorders (Kanis, 1994). Clinical implication although the evidence is far from conclusive, an exercise regimen should probably include vigorous total body exercise, including strength and aerobic training. The disease can also be prevented through proper nutrition, especially through the intake of foods rich in minerals and high in calcium and phosphorous. The adequate supply of calcium over a lifetime contributes to preventing the development of osteoporosis in patients. Published research studies show that low calcium dietary intake appears to be associated with low bone mass, rapid bone loss through osteoporosis and osteopaenia, and high fracture rates. Despite the essence of this mineral calcium, the nutrition surveys show that many people consume less than half the amount of calcium recommended to build and maintain healthy bone mineral density (Huopia et Al., 2004). Food sources of high calcium content include low-fat dairy products, such as milk, cheese, yoghurt, and ice cream; dark green, leafy vegetables, such as collard greens, broccoli, bok choy, and spinach; sardines and salmon with bones; almonds; tofu; and foods fortified with calcium, such as orange juice, cereals, and breads. Depending on how much calcium you get each day from food, you may need to take a calcium supplement. The body’s demand for calcium is greater during childhood and adolescence, and this is the phase when the skeleton is growing rapidly, as well as during pregnancy and breastfeeding. Postmenopausal women and ageing men also need to consume more calcium (Greenspan, 2007). Also the older adults are more likely to have chronic medical complications and to use medications that may impair calcium absorption. Complications Osteoporosis can have a general association with a weak bone, muscular and support system, and this may result to a variety of skeletal health conditions. Current research studies have indicated that this disease causes more than 1.5 million fractures annually in the world and the large proportion is attributed to the young individuals, aged as well as women especially those beyond the phase of menopause (Guadalupe et Al., 2009). For instance experiments show that about 50% of women and 25% of men age 50 years and above are likely to suffer an osteoporosis-related bone fractures during their lifetime. Most of these fractures associated with bone mineral loss usually occur after relatively minor falls or accidents attributed by fragility of the skeletal system and the bone. Therapeutic management and prevention of Osteoporosis The optimal goal for the treatment of osteoporosis, especially for patients who already have advanced bone loss, is to increase bone mass and bone strength to levels seen in average young women and men so as to prevent all osteoporotic fractures (Gutin and Kasper, 1992). Indeed, with the rapid aging of the population, there is an urgent need for a cure, not merely the management of osteoporosis. The clinical pharmacotherapies currently approved by the Food and Drug Administration for the management and treatment of osteoporosis includes; administration of raloxifene, estrogen, alendronate, risedronate and calcitonin. These are antiresorptive agents and their mechanism of action is based on slowing the rate of bone remodeling, and thereby, they reduce or stop bone loss. The disadvantage with these pharmacotherapies is that they are incapable of rebuilding bone, and the increase in bone mineral density in patients exposed to antiresorptive agents are not due to bone rebuilding (Greenspan, 2007). These bone mineral changes is however attributed to the result of contraction of the remodeling space and more complete secondary mineralization. The goal of treatment of osteoporosis is the prevention of bone fractures by reducing bone loss or, preferably, by increasing bone density and strength. Although early detection and timely treatment of osteoporosis can substantially decrease the risk of future fractures, none of the available treatments for osteoporosis are complete cures. In other words, it is difficult to completely rebuild bone that has been weakened by osteoporosis. Therefore, prevention of osteoporosis is as important as treatment. The following are osteoporosis treatment and prevention measures: Lifestyle changes, including quitting cigarette smoking, curtailing excessive alcohol intake, exercising regularly, and consuming a balanced diet with adequate calcium and vitamin D, using pharmacotherapeutics that reduces bone loss and increases bone strength (Bauer et Al., 1997). These includes medications such as alendronate (Fosamax), risedronate (Actonel), calcitonin (calcimar) raloxifene (Evista), ibandronate (Boniva), zoledronate (Reclast), and denosumab (Prolia). Exercise especially the weight bearing ones, has a wide variety of beneficial bone and musculoskeletal health effects. Although exercise does not bring about substantial increases in bone mineral densityits importance is subjected to the body stability and thus resulting into decreased risk of falls, as the balance is improved and/or muscle strength is increased. Osteoporosis patients should not involve themselves in straneous exercises, since their bone tissue is weak and likely to undergo fractures (Grampp et Al., 1999). Elderly patients with heart disease, diabetes mellitus, obesity and high blood pressure, have to be exposed only to exercise prescribed and monitored by physicians. Smoking of cigarettes daily throughout adult life can itself lead to loss bone mass, and is involved to decreased estrogen levels and thus bone loss in women before menopause. Prevention The most essential way of prevention of bone mineral through osteopaenia or osteoporosis loss is exposure to appropriate exercises. Most studies using specific bone-loading exercise have shown substantial increases in bone density at the specific sites loaded, but elderly people seem incapable of responding favorably to vigorous exercise. Studies have not indicated a direct relationship between exercise and estrogen therapy (Robert and Heaney, 1998). Extremely high volumes of vigorous exercise may overwhelm a person's adaptive capacity especially the aged, leading to stress fractures. For instance, young women athletes may be at a risk of suffering from menstrual dysfunction exhibit reduced bone mineral density and musculoskeletal disorders. Clinical implication although the evidence is far from conclusive, an exercise regimen should probably include vigorous total body exercise, including strength and aerobic training. The disease can also be prevented through proper nutrition, especially through the intake of foods rich in minerals and high in calcium and phosphorous. The adequate supply of calcium over a lifetime contributes to preventing the development of osteoporosis in patients (Amory, 2004). Published research studies show that low calcium dietary intake appears to be associated with low bone mass, rapid bone loss through osteoporosis and osteopaenia, and high fracture rates. Despite the essence of this mineral calcium, the nutrition surveys show that many people consume less than half the amount of calcium recommended to build and maintain healthy bone mineral density. Food sources of high calcium content include low-fat dairy products, such as milk, cheese, yoghurt, and ice cream; dark green, leafy vegetables, such as collard greens, broccoli, bok choy, and spinach; sardines and salmon with bones; almonds; tofu; and foods fortified with calcium, such as orange juice, cereals, and breads (Ebeling, 2008). Depending on how much calcium you get each day from food, you may need to take a calcium supplement. The body’s demand for calcium is greater during childhood and adolescence, when the skeleton is growing rapidly, and during pregnancy and breastfeeding. Postmenopausal women and older men also need to consume more calcium. Also, as you age, your body becomes less efficient at absorbing calcium and other nutrients. Older adults also are more likely to have chronic medical problems and to use medications that may impair calcium absorption. Conclusion Osteoporosis is a disease characterised by loss of the bone mineral density and this leads to fragility and a subsequent development of fractures. This is a preventable disease of the skeletal system and its management especially the achievement of complete healing can not be attained. Despite this poor prognosis to pharmacotherapeutic remedies, the disease can be prevented by good mineral intake such as calcium and phosphorous, proper excercising, change in poor lifestyle including high alcohol consumption and cigarette smoking, and using hormonal therapies. Food high in calcium should be provided to the growing populations as their needs for this mineral is high. References Amory, J. K.(2004). Exogenous testosterone or testosterone with finasteride increases bone mineral density in older men with low serum testosterone. J Clin Endocrinol Metab 89: 503-10. Bauer DC, Gluer CC, Cauley JA, Vogt TM, Ensurd KE, Genant HK, et al (1997), Broad band ultrasound attenuation predicts fractures strongly and independently of densitometry in older women .A prospective study of osteoporotic fractures research group. Arc Intern Med;157:629-34. Benito M (2005), Effect of testosterone replacement on trabecular architecture in hypogonadal men. J Bone Miner Res; 20(10):1785-91. Ebeling PR (2008), Clinical practice. Osteoporosis in men. N Engl J Med; 358(14): 1474-82. Grampp S, Henk CB ,Fuerst TP, Lu Y, Bader TR, Kainberger F, et al (1999), Diagnostic agreement of quantitative ultrasonography of the calcaneus with dual X Ray absorpsiometry of spine and femur. Am J of Roentgenology 1999;173:329-34. Greenspan SL, Bone HG, Ettinger MP, Hanley DA, Lindsay R, Zanchetta JR, et al., (2007), Effect of recombinant human parathyroid hormone (1-84) on vertebral fracture and bone mineral density in postmenopausal women with osteoporosis: a randomized trial. Ann Intern Med.;146(5): 326-39. Greenspan SL, Nelson JB, Trump DL and Resnick NM (2007), Effect of once-weekly oral alendronate on bone loss in men receiving androgen deprivation therapy for prostate cancer: a randomized trial. Ann Intern Med.;146(6): 416-24. Guadalupe-Grau A, Fuentes T, Guerra B, Calbet JA (2009), Can Vigorous Excercise Play a Role in Osteoporosis prevention? A Review: Journal Sports Med. ;39(6):439-68 Gutin B, and Kasper MJ (1992), Can vigorous exercise play a role in osteoporosis prevention? A review. Journal on Osteoporos Int. ;2(2):55-69 Huopio J, Kroger H, Honkanen R, Jurvelin J, Saarikoski S, Alhava E. (2004), Calcaneal ultrasound predicts early postmenopausal fractures as well as axial BMD. A prospective study of 422 women. Osteoporosis - Int; 15:190-5. Kanis JA (1994), Assessment of fracture risk & its application to screening for postmenopausal osteoporosis; Synopsis of a WHO report. WHO study group. Osteoporosis Int ;4;368-81. Khan AA, and Syed Z (2004), Bone densitometry in premenopausal women: Synthesis and review. J Clint Desitm; 7:85-92. Khosla S (2010), Update in male osteoporosis. J Clin Endocrinol Metab ;95(1):3-10. This is an excellent new overview of this topic. Lewiecki EM (2004), Management of osteoporosis Clinical and Molecular Allergy; 2:9. MacLean C, Newberry S, Maglione M, McMahon M, Ranganath V, Suttorp M, et al., (2008), Systematic review: comparative effectiveness of treatments to prevent fractures in men and women with low bone density or osteoporosis. Ann Intern Med;148(3): 197-213. Marshall D, Johnell O, and Wedel H (1996), Meta Analysis of how well measures of bone mineral density predicts occurrence of osteoporotic fractures. BMJ; 312:1254-59. Melton LJ 3rd, Crischilles EA, Cooper C, Lane AW, Riggs BL (1992), How many women have osteoporosis? J Bone Miner Res; 7:1005-10. Nelson HD, Helfand M, Woolf SH, Allan JD (2002), Screening of post menopausal osteoporosis: A review of the evidence for the U.S. preventive services task force. Ann Intern Med; 137:529-41. Riggis BL, Melton LJ 111 (1995), The worldwide problem of osteoporosis ; insights afforded by epidemiology. Bone; 17 (5 suppl):505 S-511 S. Robert P, Heaney MD (1998), Bone mass, Bone loss and Osteoporosis Prophylaxis. (Editorial). Ann Intern Med; 313-4. Siris ES, Miller PD, Conner EB, Faulkner KG, Wehren, Abott TA, et al. (2001), Identification and fracture outcomes of undiagnosed low bone mineral density in postmenopausal women. JAMA; 286:2815-2822. Read More
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