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S. M.
Pathology Report
July 17, 2006
Osteoporosis
Osteoporosis is a disease of the skeleton identified by low bone mass and deterioration of the micro architecture of the bone (Sambrook & Cooper, 2006). The main two reasons this disease develops are the following: poor development of peak bone mass in the early years of life and age related bone loss as the years progress (Downey & Siegel, 2006). The increased fragility of the bones is directly related to an increased risk of bone fracture (Sambrook & Cooper, 2006).
Peak bone mass begins to develop early in life and is influenced by genetics, diet, and exercise. As an adult, bone mass is determined by the rate at which some bone cells are resorbed and new bone cells generate (Kessenich, 2006). At the cellular level, bone loss occurs because of an imbalance between the activity of osteoclasts and osteoblasts. In adults, bones constantly remodel in a sequence of bone resorption and bone formation (Sambrook & Cooper, 2006). When the number of cells resorbed is greater than the number of cells generated, osteoporosis occurs (Kessenich, 2006). If these remodeling and resorption cycles are not balanced, and remain untreated, the problem will become larger by a rise in the rate of initiation of new bone remodeling cycles causing the bones to become weaker and more fragile. Estrogen plays an important role in the remodeling of bones; osteoporosis is most common in postmenopausal women. With menopause, the decreased level of estrogen causes a remodeling imbalance, which leads to bone loss. The bone loss also occurs due to other age related causes i.e. secondary hyperparathyroidism and a sedentary life style (Sambrook & Cooper, 2006).
More than 9.4 million women have lost more than 25% of their peak bone mass (Downey & Siegel, 2006). Among Caucasians, about 50% of women and 20% of men, over the age of 50, will have a fracture due to osteoporosis. Fractures from osteoporosis are highest for Scandinavian and North American women, while women residing in southern Europe have a risk level that is seven times lower. Asian and Latin American people are also at a lower risk. Worldwide, fracture risk increases with the decrease in bone mass and the increase in the incidence of falls that comes with advancing age (Sambrook & Cooper, 2006).
Various risk factors for osteoporosis include low estrogen levels in women, oral glucocorticoid therapy, family history, diet, low body mass index, smoking, alcohol abuse, and lack of exercise. Aromatase inhibitors, often used in the treatment of breast cancer, are also associated with bone loss (Compston, 2006). Doctors can combine these risk factors to determine the probability of hip or other fractures. To reduce the risk of fractures, it is crucial to know the risk factors and take preventive measures (Sambrook & Cooper, 2006).
Osteoporosis can be placed into two categories: primary and secondary. Primary osteoporosis is defined as bone deterioration associated with advancing age and low hormone levels. Secondary osteoporosis is attributed to chronic conditions that lead to bone loss such as hyperthyroidism and long term use of certain medications such as glucocorticoids (Downey & Siegel, 2006).
The adverse outcomes of osteoporosis can be placed into three categories: mortality, morbidity, and cost. Most patients survive after a fracture, but the hip fracture is the most serious, with ten to twenty percent mortality in the first year, with risk of death being greatest in the first six months. However, most deaths are not directly attributed to the fracture; instead, they result from infections and other age related complications. Because death is a very real possibility, early detection is important (Sambrook & Cooper, 2006).
Bone mineral density is an excellent measure of bone strength, as well as the macro architecture (size and shape), micro architecture (trabecular and cortical), damage accumulation, at rate of bone turnover. The density of adult bones is the compilation of peak bone mass accumulated before birth, and during childhood and adolescence. Although genetics plays a critical role in the development of peak bone mask, the importance of environmental factors such as diet and exercise can not be understated. People with high peak bone mass have less osteoporatic bone loss. Bone mineral density is an important measurement for assessing the risks of developing osteoporosis (Sambrook & Cooper, 2006).
Dual-energy x-ray absorptometry (DXA) scanners measure bone mineral density and determine if osteoporosis is present by using a bone density T score at the spine, hip, or forearm. The World Health Organization defines osteoporosis as a T score of -2.5 or less (Fogelman & Blake, 2005). With a T score of -2.5 or less the risk of fractures is high, and the lower the score the higher the risk (Compston, 2006). DXA testing is fast and allows for early and accurate assessment of osteoporosis (Kessenich, 2006). Those who should have a DXA scan are those who are at high risk for developing osteoporosis and those over the age of seventy, especially women (Compston, 2006).
Osteoporatic fractures usually occur in the hip, distal forearm, and vertebral body; individuals who obtain a fracture are at risk of yet another fracture. However, osteoporosis is not limited to these locations, it affects the entire skeleton. The most devastating fractures are in the hip because they require hospitalization, cause severe disabilities, and can lead to death. Hip fractures are usually the result of a fall; eighty percent are in women and ninety percent are in those over the age of fifty. Unlike hip fractures, some osteoporatic fractures are not usually the result of an injury such as a fall (Sambrook & Cooper, 2006).
Vertebral fractures do not occur as often as hip fractures, and about one third that are identified are never brought to the attention of a specialist, although they can cause considerable pain, disability, and thoracic kyphosis. Vertebral fractures typically occur during everyday activities, such as bending or lifting light items; less than one fourth is the result of a fall. They happen in men as often as in women, unlike wrist fractures that typically occur in women (Sambrook & Cooper, 2006).
Fractures in the distal forearm have an increased pattern of occurrence in white women over the age of forty-five. Most of these fractures are in those of sixty-five years and older. The incidence of wrist fractures is low in men, and the risk does not increase with age (Sambrook & Cooper, 2006).
Regardless of the age of the man or woman with an osteoporatic fracture, he or she is at increased risk of other fractures in the future. Patients with a vertebral, hip, or wrist fracture are ten times more likely to develop another fracture in the same area. They are two to three times more likely to develop fractures in other locations (Sambrook & Cooper, 2006).
Most fractures are the results of falls, so taking measures to prevent falls seems to be an obvious decision. No studies show that such strategies work; however, the use of hip protectors to reduce impact has proven very effective. Of course, patient compliance is a must if the hip protectors are to have the desired result (Sambrook & Cooper, 2006).
Patient compliance also is imperative if exercise is to be used as a means of preventing or treating osteoporosis. When patients lift weights, a mechanical strain is placed on the bones. The bones then respond to the strain by increasing cell metabolism and collagen synthesis. Studies have shown that within days of a single session of weight bearing exercise bone cells changed into active osteoblasts. With continued exercise, bone strength is increased (Downey & Siegel, 2006). To enhance their chances of creating stronger bones, the osteoporatic patient should combine exercise with medications.
Preventive drugs can be considered in how they act on the bone. Antiresorptive agents act on bone resorption, they include calcium, vitamin D, hormone therapy, bisphosphonates, and calcitonin. An anabolic agent, such as parathyroid hormone, acts on bone formation (Sambrook & Cooper, 2006). The most common cause of osteoporosis in women is decreased levels of estrogen; therefore, many times hormone replacement therapy (HRT) is attempted.
HRT is effective in slowing down bone loss and allowing bone mineral density to increase. Although this therapy is promising, serious risks are associated with HRT. Increased risks of endometrial cancer, breast cancer, coronary heart disease, and pulmonary embolism exist while using this therapy. HRT is usually reserved for women who also need relief from the symptoms of menopause. The risks need to be weighed against the benefits, and perhaps other avenues should be followed for treatment (Downey & Siegel, 2006).
Calcium supplements alone have little effect on bone mineral density. Low levels of vitamin D have been associated with hip fractures and low bone mineral density (Sambrook & Cooper, 2006). Vitamin D enhances calcium absorption and inhibits parathyroid hormone synthesis and secretion (Downey &Siegel, 2006). Calcium taken with vitamin D has been found to effectively increase the bone mineral density in the hips of postmenopausal women (Compston, 2006). If estrogen is taken with calcium and vitamin D the benefits are increased but only slightly. Recall however, there is increased risk of stroke and cardiovascular problems while taking estrogen, especially in women over the age of seventy; therefore, attempts at other therapies should be made (Sambrook & Cooper, 2006).
The biggest advancements in treating osteoporosis in recent years have been with bisphosphonates, which work by inhibiting the osteoclasts, which are the cells that cause the break down of the bones. Bisphosphonates have been shown to reduce the risk of hip fracture by twenty to forty percent and reduce vertebral fractures by forty to fifty percent (Kessenich, 2006). Alendronate and risedronate reduce the risk of spinal fractures in women with low T scores. Ibandronate is specifically approved for preventing vertebral fractures. These drugs required the patient to fast and remain upright for 30 minutes after taking a dose; also, they can cause upper gastrointestinal side effects. Therefore, they were reformulated into once a week or once a month dosages. Despite the benefits of these bisphosphonates, there are concerns about their long term effect because these drugs remain in the skeleton for years. Bisphosphonates work to reduce bone resorption, while anabolic agents work to stimulate bone formation (Sambrook & Cooper, 2006).
Such an anabolic agent is parathyroid hormone (PTH); trials have shown a sixty-five percent reduction in the risk of vertebral fractures and fifty-three percent reduction in all other fractures (Sambrook & Cooper, 2006). PTH is secreted by the parathyroid gland and controls calcium homeostasis by regulating the amount of calcium released from the bone and its resorption. PTH influences the number of osteoclasts and their activity. It has been shown that as intracellular calcium increases so does the number and activity of osteoblasts (Downey & Siegel, 2006). The disadvantage of this therapy is the benefits go down when treatment is stopped unless it is followed up by an antiresorptive agent. Fortunately, researchers are working to advance new treatments (Sambrook & Cooper, 2006).
One such new treatment is strontium renelate, approved to treat osteoporosis in Europe but not the United States. It works to increase bone formation and decrease bone resorption in postmenopausal women. It has been shown to reduce the risk of vertebral fractures by fifty-two percent. It is generally well tolerated, but there is an increased risk of venous thrombosis. In the future, this drug could be an alternative to bisphosphonates (Sambrook & Cooper).
Currently, bone research continues to investigate the pathogenesis of osteoporosis in order to develop more effective preventive and treatment regimens (Kessenich, 2006). A better understanding of cytokines, prostaglandins, and how mechanical loading influence the break down and build up of bones will lead to new developments and relief for suffers (Downey & Siegel, 2006).
References
Compston, J. (2006, March). Need to Know – Osteoporosis. PulseClinical, 84, 44-46. Retrieved July 6, 2006, from Ebsco database.
Downey, P., & Siegel, M. (2006, January). Bone Biology and the Clinical Implications for Osteoporosis. Physical Therapy, 86(1), 77-91. Retrieved July 6, 2006, from Ebsco database.
Fogelman, I., & Blake, G. (2005, December 17). Bone densitometry: an update. The Lancet, 366(9503), 2068-2070. Retrieved July 6, 2006, from Ebsco database.
Kessenich, C. (2006, February). Osteoporosis. Nurse Practioner, 31(2), 44-47. Retrieved July 6, 2006, from Ebsco database.
Sambrook, P., & Cooper, C. (2006, June 17). Osteoporosis. The Lancet, 367(9527), 2010-2018. Retrieve July 6, 2006, from ProQuest database.