Osteoporosis: The Brittle Bone Disease

Online Course #9006 or #5006 - 10 Contact Hours
Author: Peggy M. Goulding, Ph.D.
Editor: Shelda L. Shank, RN, BSN, PHN
© National Center of Continuing Education, Inc.

For your convenience, this course has been divided into 2 sections:
Below is Part 1 of 2.
Table of Contents …Part 2 …Independent Analysis …Evaluation

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Purpose and Goals

The purpose of this course is to provide a comprehensive overview of osteoporosis for nurses and other healthcare professionals. Emphasis is on an understanding of the life-long risk factors for the development of the disease, particularly those that reflect lifestyle choices. New treatment approaches are outlined based on medical research. Consideration is also given to the unique challenges presented by osteoporosis in men.

Instructional Objectives

Upon completion of the course, the learner will be able to:

1. Identify the two types of bone tissue and their anatomical distributions.
2. Outline the physiological sequence of events resulting in osteoporosis.
3. Define the role of the "skeletal storehouse" in maintenance of the body's calcium balance.
4. Name three health conditions that can increase risk for development of osteoporosis.
5. List five lifestyle factors contributing to the risk for osteoporosis.
6. Identify the prevalence and risk factors for development of osteoporosis in men.
7. Outline current methods and criteria for the diagnosis of osteoporosis.
8. List the primary pharmacological approaches to osteoporosis treatment.
9. Outline current and potential approaches to osteoporosis prevention and treatment, including use of nutrition and nutritional supplements.
10. Identify ways to minimize fractures in patients with osteoporosis.
11. List key topics for the nurse to address in patient education.

Introduction

Leaning heavily upon her cane, the elderly woman strained to look upward. It was difficult since her head jutted sharply forward from her body and her back was twisted and bent. An ungainly dowager's hump pulled her jacket tight across her drooping shoulders. Every day, thousands like her hobble about their homes, struggle to climb stairs, brave boarding a bus or shuffle along the streets, fearful that a stumble will lead to a fracturing fall. Age and a long life have not brought them freedom to enjoy their remaining days; instead, they are burdened by the visible evidence of their frailty and robbed of their independence. They are victims of the most common bone disease in the world, osteoporosis. One of the least understood and most hotly debated chronic degenerative diseases in medical science today, its actual cause is not fully known, although numerous theories abound.
This serious public health problem, whose name literally means porous or brittle bones, afflicts over 29 million Americans. Millions more currently have the disease but don't know it, as the symptoms are most times undetectable until a bone breaks. Osteoporosis causes 1.3 million fractures a year and costs the nation $13.8 billion annually. Since 1900, the number of Americans over the age of 65 has quadrupled. With the development of antibiotics, vaccines, enhanced nutrition, improved sanitation and food processing, many diseases have been eradicated. As a result, life expectancy has increased dramatically, now reaching the predicted age of 79 for women and 74 for men. Twelve percent of the U.S. population is now 65 years of age or older: that's approximately 35 million senior citizens, and that proportion is expected to reach 20 percent by the year 2030. Seniors 75 years of age and over are the most rapidly growing group in our society.
In correlation with the increase in life expectancy, the rate of age-related illnesses has also increased. These illnesses include vascular diseases of the heart, brain, and limbs; certain types of cancer; Alzheimer's disease; and osteoporosis. Recent information obtained from the occupational therapy division of the Swezey Institute reported that every year, osteoporosis is responsible for more than 275,000 hip fractures, 500,000 vertebral fractures, 200,000 wrist fractures and at least 300,000 fractures at other sites. Fractured hips are the leading cause of accidental death in people over 75 years of age and the second leading cause of death in those aged 45 to 74. Nearly two million Americans over the age of 65 will fracture their hips this year, and 15 to 30 percent of them will die within one year of their injury due to complications associated with their immobility. To put these numbers into perspective, more women are likely to die from an osteoporosis-related fracture than from breast, cervix and uterine cancer combined. Of the survivors, more than 40 percent will be unable to get around or care for themselves without mechanical aids or someone's help. Approximately 15 to 25 percent will be confined to skilled nursing facilities, where they will remain for the rest of their lives.

History of Osteoporosis: Facts and Figures

Although British surgeon Sir Astley Cooper wrote in 1824 that the skeleton seemed to become more fragile with age, osteoporosis was not fully described in medical texts until the mid 1920's. After the discovery of X-rays in 1895 by the German physicist, Wilhelm Roentgen, treatises on fractures in weakened bones began appearing in the German medical literature. In 1941, Boston endocrinologist Fuller Albright explored the increased bone breakdown after menopause, but his findings drew little attention since the American medical community, like the public at large, was focused on more immediate issues: fear of polio epidemics was rampant; pneumonia was a lethal killer; and syphilis and TB were medically uncontrollable cripplers. Even after the discovery of antibiotics, public attention was directed toward two other dramatic killers, cancer and heart disease. The incidence of osteoporosis was increasing right along with life expectancy, but an awareness of its seriousness didn't keep pace with the threat it posed to the health and well being of the elderly.
Post-menopausal osteoporosis was first described in the 1940s but financial backing for research projects was slow to come. In 1965, a landmark conference, sponsored by the World Health Organization (WHO) and the National Institutes of Health (NIH), formulated a worldwide epidemiological study of osteoporosis giving recognition to the seriousness of the problem. In 1984, the National Institutes of Health publicized this disease, citing it as a significant threat to health and emphasizing that bone loss could be reduced by estrogen therapy, calcium, good nutrition and exercise. These findings were expanded in a 1987 conference sponsored by the NIH and the National Osteoporosis Foundation. Just ten years ago, only about 15 percent of Americans knew about this disease. Today, over 85 percent do. In view of the latest research and information, osteoporosis should be viewed as a largely preventable disease.

Bone Basics

Most people don't think about skeletons except at Halloween or to worry about one tucked away in a closet, so it is easy to take our skeletal health for granted. The human skeleton is like the super-structure of a building with its framework supporting and protecting the organs of the body. Bones are functional in design, and vary depending on location and intended use. Protective bones like the skull and pelvis are thick, while arm and leg bones are long, hollowed out cylinders that combine lightness with strength. Engineers recognize the cylinder as the geometric form best able to withstand forces from above and below (compression), as well as twisting and bending forces (torsion). The leg bones can endure a tremendous amount of pressure from running and jumping, while resiliency is the primary characteristic of the 24 vertebrae.
Bone is composed of collagen, a leathery protein material which differs from the collagen found in other parts of the body. Chains of peptide molecules make up the bone collagen, and they are bound around each other in long strands in the base material of the bone. These strands are stacked together like a wall of bricks, with tiny openings within which calcium and phosphorus crystallize. Calcium ions are small, but when placed in a latticework of crystals, they form a huge surface area. Ninety-nine percent of the body's calcium is held in the bones, and it combines with phosphorus, hydrogen and oxygen to form crystals called hydroxyapatite, which resemble table salt crystals. This gives it hardness and structural integrity. Bone crystals also contain sodium, potassium, magnesium, strontium, carbon and chlorine. Without these minerals, collagen would be like a pile of spaghetti and not at all like bone.
Separately, neither collagen nor the crystals are durable; but together, they are amazingly strong. Skeletal growth goes on until age 18; after that age, the bones continue to add 10 to 15 percent to their density, becoming thicker and wider. Bones are heaviest and strongest around age 35, at which point they make up about 10 percent of the body weight.
Bone tissue is arranged in two different ways. Some is densely packed into compact layers forming a tough outer shell called the cortex. Eighty percent of the skeleton is this hard bone. The remaining 20 percent is woven into a meshwork of thick, tough plates called trabecular bone. This spongy, porous tissue fills the inner cavities of the bones, which also contain marrow and fat. Cortical bone receives added strength from tightly packed rods called Haversian systems. Their canal-like walls are hardened with minerals and are usually too narrow for blood cells to pass through, but fluids and ions are able to circulate freely. Due to this continuous movement and chemical activity, bone tissue is able to replace itself completely about every seven years. The overall structure remains fairly constant, but the tiny mineral crystals and molecules that compose it are replaced.
Bone serves as a reservoir of essential minerals for the rest of the body, and it attracts other elements such as lead and mercury which are toxic. The bones take up and bind fluoride, the same substance that most communities add to their drinking water to prevent dental caries. By measuring strontium in excavated bones, anthropologists and archaeologists have learned facts about the eating habits of ancient man and animals, since meat eaters accumulate less of this element than vegetable eaters do. In modern day nuclear tests or accidents, large amounts of radioactive strontium reach the bone and remain there, destroying bone tissue over a long period of time.
While 99 percent of all calcium is in the bones, the remaining one percent is spread throughout the body and is crucial to the proper functioning of all organs. Calcium is necessary for the smooth performance of all body systems. Circulating in the bloodstream, it is available to energize countless electrical impulses and chemical reactions that operate the heart, brain and other organs. Muscle cells cannot contract without it, nerve cells cannot send impulses without it, and it's needed for blood to clot. Dangerously low levels of calcium can cause life-threatening seizures, organ malfunctions and abnormalities in the heartbeat. It is so important that the body has a specific mechanism for keeping available calcium at an appropriate level at all times.
Bones are effective reservoirs, supplying calcium when tissues need it and acting as a dam when the tissues are getting too much. If the concentration in the blood begins to fall, the bones release more calcium to make up for the deficit. If the concentration gets too high, the bones extract the excess. There is a state of dynamic equilibrium in which the calcium is always moving in one direction or another to maintain a constant level in nonskeletal tissue.
Food and dietary supplements are the body's only outside sources of calcium, and enough must be consumed and absorbed to maintain normal blood levels. However, in the United States, there is usually an insufficient calcium intake, which places the bony framework in jeopardy. This deficiency is particularly dangerous in growing children, adolescents and people over 45 years of age, since all need to gain calcium while maintaining their bone tissue. Seventy percent of the bone mass is accumulated in the three to four year growth spurt during the teenage years, and additional bone is built up until around age 35. When the blood level of calcium is low, the intestine will absorb more and the kidneys will eliminate less. If this does not provide an adequate amount, the skeletal storehouse will be called upon to supply more of the needed mineral.
Three hormones play an important role in this complicated biological process: 1) parathyroid hormone (PTH), 2) calcitonin, a peptide hormone and 3) hormonal Vitamin D. One medical expert called the effects of these three hormones "an exquisite control system." As the blood calcium level falls, PTH is excreted by the parathyroid gland to speed up bone breakdown. If the blood level becomes too high, the amount of PTH will drop. Calcitonin is a hormone produced by specialized cells within the thyroid gland, and it acts to conserve calcium in the bones by blocking the effects of PTH. Vitamin D is produced in skin tissue during exposure to the sun's ultraviolet rays; then this "sunshine" vitamin must be chemically converted in the liver and kidneys into an active form. The end substance stimulates calcium absorption in the intestine.
The PTH secreted by the parathyroid glands also helps protect against low blood calcium levels by increasing the activation of Vitamin D by the kidneys. If there is little exposure to sunlight, a dietary deficiency, or kidney or liver disease, the resulting deficiency in Vitamin D causes abnormally low levels of magnesium and phosphorus, and insufficient calcium for bone growth and maintenance. In menopause, the kidney also loses some of its ability to convert Vitamin D into its active form. The price paid for maintaining a constant level of calcium in the blood is a loss in bone quality and strength.

Hormones that Regulate Calcium Levels in the Blood

Parathyroid Hormone (PTH)

• Secreted by parathyroid glands in the neck.
• Activated by low levels of blood calcium.
• Stimulates bone resorption - increases release of calcium from bones.
• Acts on kidneys to: 1) reduce calcium loss in urine. 2) convert Vitamin D to an active chemical form that stimulates absorption of calcium in the intestine.

Calcitonin

• Produced by thyroid gland.
• Activated by high levels of blood calcium.
• Blocks bone resorption and reduces the release of calcium from bones.

Vitamin D

• Is not just a vitamin since it is produced in skin cells during exposure to ultraviolet rays from the sun.
• Must be converted to its active chemical form by the liver and kidneys before it works.
• Stimulates calcium absorption from the intestine.

Remodeling
The hormones that are involved in the maintenance of calcium blood levels are also part of a chemical process that controls bone growth and repair. There is a constant tearing down and rebuilding of the skeleton that occurs in millions of sites within the bones.
In the late 1800's, a German orthopedic surgeon named Julius Wolff formulated a theory of bone transformation now known to the world as Wolff's Law: Bone accommodates the forces applied to it by altering its amount and distribution of mass. It refers to the process by which bone elements arrange themselves and grow larger or smaller in an orderly manner as they constantly tear down and rebuild, shaping new growth in response to stress. This renewal process, called remodeling, enables bones to repair themselves and to release vital calcium into the bloodstream.
Bone deposit and resorption occur at the outside and the inside surfaces of the bone, called the periosteum and the endosteum respectively. Osteoblasts and osteoclasts are the cells responsible for the remodeling of bone. Osteoblasts are the cells responsible for bone deposit, and osteoclasts are responsible for resorption of bone.
If bones undergoing remodeling in the resorption phase were magnified, their surface would look like potholed pavement after a hard winter. The osteoclasts are busily tearing up the surface, creating craters for the busy osteoblasts to patch. Osteoclasts are related to macrophage cells, and their precursors originate in the bone marrow and circulate through the blood. The osteoclasts migrate to specific bone sites and create an acid environment in which the calcium is dissolved. Like PacMan®, they chew away at the bone surface as enzymes dissolve the bone matrix of collagen and proteins. One large osteoclast can remove an area twice its size in 24 hours. Researchers are now exploring the means by which the osteoclasts are able to establish the acid environment that is essential for bone erosion. The calcium dissolved in the process passes into the bloodstream.
The second phase of remodeling of bone, the formation of new tissue, begins when osteoblasts migrate to the sites where bone was resorbed by the osteoclasts, and they go into action to produce collagen and begin the repair work. Osteoblasts form a closely packed sheet on the surface of the bone, from which cellular processes extend through the developing bone. After they lay down the basic bone structure, the osteoblasts are engulfed by the growing bone matrix; as the material calcifies, the cells are trapped and can no longer lay down new bone. They then develop into osteocytes, stable bone cells that regulate the finishing stages of bone production. Lawrence Raisz, of the University of Connecticut Health Center in Farmington, says that over the years, all of the bone in a person's body will be replaced. But the amount of bone surface being remodeled at any one time is small, probably only about five percent. This turnover occurs at specific sites throughout trabecular bone, while cortical bone remodeling occurs only along its border with the marrow and near the Haversian canals that penetrate it. The entire process from the initiation of resorption to the completion of repair takes about 100 days. Normally, the balance between the two determines whether bone tissue accumulates or disappears. With advancing age, the constant remodeling jeopardizes the skeleton as bone reformation lags behind bone loss.
Bones become fragile as a result of reduction in bone mass and density, and reduction in the effectiveness of trabecular cross-bracing. If there is a reduction in bone connectivity, and impact from a mechanical load occurs, then the bone will fracture. Loss of bone connectivity occurs with aging; the loss is greater in women than in men, and is greater still in individuals with osteoporosis. Once this bone fatigue occurs, the osteoclasts begin a process called apoptosis, or programmed cell death, and the bones no longer are able to repair damage. Matrix quality is also a factor, and a reduction in the degree of cross linkage is associated with a loss of bone strength. Low serum copper and low calcium intake appear to be associated with poor cross-linkage within the bones.
Other important causes of bone fragility are a high level of bone remodeling and factors relating to bone geometry. The hip axis length and hip angle affect risk of fracture independent of bone mass, and some data suggest that differences in hip axis length may help to explain the differences in fracture prevalence between Japanese and Caucasian populations, for example. Treatments to protect or increase bone mass will reduce fracture; non-mass factors, which also make an important contribution to skeletal strength and reduced susceptibility to bone fragility, need further investigation.

Aging and The Skeletal System
Age disrupts the dynamic equilibrium between the skeleton and the rest of the body. As the body slowly and silently wastes away, tissue is lost from within, progressively thinning the bones' walls and framework. With advancing age, both cortical and trabecular bone are lost, and the rates are highest in women around the time of menopause. Women lose 30% to 50% of trabecular bone mass, and 25% to 30% of cortical bone mass; losses in men are on the order of 15% to 45% and 5% to 15% for trabecular and cortical bone, respectively.
With osteoporosis, the natural loss of bone that accompanies aging is accelerated to abnormal, critical levels. The bones become weaker, thinner and more brittle with a marked increase in susceptibility to fracture. The skeletal framework can no longer withstand sudden or even normal mechanical stresses, and fractures occur. Often, the first warning signal is a fractured wrist. Until the age of 45, this type of fracture occurs equally between the sexes. But after 45, ten times as many women as men break their wrists. In 1882, German surgeon Paul Bruns was the first to observe in print that fractured wrists occurred more often in older women, claiming they tripped over their long skirts. We know better today.
Everyone begins losing bone mineral at around 40 years of age, but women who haven't been pregnant are at the greatest risk of suffering the fractures that are a major symptom of osteoporosis. Cortical bone is lost continuously and evenly by both sexes, but after menopause, women lose this tissue twice as fast as men. One expert stated, "Osteoporosis is not a disease like tuberculosis that the patient either has or does not have." Mayo Clinic studies show that one-half of all elderly women eventually suffer fractures due to osteoporosis.
Trabecular bone is destroyed quickly and by the age of 80, osteoporotic women have lost more than half of their trabecular bone tissue. The vertebrae are mainly composed of trabecular bone, and they can become compressed like so many crushed shredded wheat biscuits. The vertebrae of the upper spine often collapse more in the front and become wedge shaped, bending the upper spine forward and causing the back to hunch over. When an entire vertebra is damaged, the "crush" fracture may be painful and take several months to heal. Rest, analgesics and "tincture of time" are usually the best treatments. Some women may experience several essentially asymptomatic compression fractures, and only become concerned when they develop a hunched back and round shoulders, and notice dropping hemlines which emphasize their loss of height. This can be a dramatic change, sometimes three to eight inches. The osteoporotic vertebrae, particularly those in the lower back which bear the most weight, eventually shrink and collapse, sometimes because of the simple act of standing or sneezing. The ordinary physical efforts required in everyday life - picking up a lightweight bag of groceries, bending over, climbing stairs, or just turning over in bed - can cause a compression fracture.
The collapse of multiple vertebrae over a period of time leads to shrinkage of the entire spinal column. As the spine shortens, it bends forward, shortening the chest and causing the lower ribs to rest upon the bones of the pelvis. Breathing becomes difficult and many people complain of shortness of breath, with lung infections becoming a danger. The abdomen, also compressed, bulges and digestive problems are common. Over 1/3 of the women with collapsed vertebrae develop a curvature of the lower spine which causes pain and stiffness, making a tortured ordeal of many ordinary movements.
Deforming though they are, these vertebral fractures rarely threaten life. The most common cause of fatal fractures among the elderly is a fall from a standing height or less. At least 1/3 of the nation's elderly fall each year, and those aged 65 and up make up 3/4 of all fatal falls recorded. Most deadly slips and tumbles happen indoors and only a surprising eight percent are caused by missteps in snow or on ice. A fall from a standing height in a person with normal bone density will usually provoke nothing more than a surprised look and maybe a few bruises. But in an individual with osteoporotic bones, a spill is likely to result in a fractured hip or back.
The broken bone itself is not as dangerous as the long period of inactivity required for healing, with the ever-present potential for complications such as pneumonia, pulmonary embolism, decubiti, urinary infection, depression and malnutrition. Many fractures result in a death that could have been avoided by a reduction in bone loss.

The Role of Estrogen and Other Hormones in Bone Biology
Preserving a balance between bone resorption and reformation is the key to maintaining bone mass, with osteoporosis being the consequence of an imbalance between the two. Estrogen has been shown to have a role in the bone remodeling process. The cellular action of estrogen is mediated by estrogen receptors in both osteoclasts and osteoblasts. It acts through these receptors to regulate the process of apoptosis, or programmed cell death. Estrogen accelerates the death of osteoclasts, while prolonging the life of osteoblasts. In postmenopausal women between the ages of 50 and 60, there is a decrease in estrogen levels; bone resorption increases and the formation process cannot keep up. Bone replacement with new tissue will be slowed and bone mass will be gradually decreased.
Estrogens also have striking positive effects on the intestinal absorption of calcium and the reabsorption of calcium from the renal tubule, thus promoting a positive calcium balance. Menopause and decreased estrogen levels are associated with intestinal resistance to Vitamin D. Reduced estrogen levels at menopause can thus result in calcium deficiency, which in turn affects bone health.
The thyroid hormones, thyroxine (T4), and triiodothyronine (T3), also influence the formation of bone as they can speed up remodeling. An overactive thyroid gland can cause bone loss as can taking too much thyroid medication.
Steroids are hormones produced by the testes, ovaries and adrenal glands. Some sex hormones help maintain bone and prevent osteoporosis by exerting a protective effect on the osteoblast cells; others in this complex group contribute to the disease process, apparently by weakening these cells and hastening cell death, and many of their functions are in opposition to each other. Cortisone and the related glucocorticoids have been shown to cause osteoporosis, by mechanisms such as reducing calcium absorption, increasing calcium excretion, and limiting production of the gonadal hormones. Estrogen, as described above, and progesterone block the resorption of calcium in the bones and have an effect upon the adrenal glands' production of the bone destroying hormones mentioned above. Estrogen also triggers the release of the bone-conserving hormone calcitonin, which helps form liver hormones that block the cortisone-like steroids from resorbing bone. In addition, it prevents the action of PTH while interacting with the growth hormone, thyroid hormones and others. Testosterone, produced by the testicles and in lesser amounts by the adrenal glands, preserves bone and offers some protection to counter the loss of estrogen in women as well as in men.

Are You At Risk?

Physical Factors

• Caucasian or Asian
• Thin and petite
• Had an early menopause - or have never been pregnant
• Female
• Over 35 generally
• Fair skinned
• Family history of osteoporosis
• Have gastrointestinal disorder
• Have an illness that causes inactivity
• Have an overactive thyroid gland
• Are amenorrheic or anorexic
• Life Style and Dietary Factors
• Smoker
• Regular alcohol intake
• Take a bone-wasting drug
• Do not have an adequate calcium intake
• Consume five or more cups of coffee a day
• Do not exercise regularly
• Consume a lot of carbonated beverages
• High protein and phosphorus intake
• High fat intake
• Consumption of antacids containing aluminum

Risk Factors for Osteoporosis

There are still many unknown facts about osteoporosis, but certain risk factors now associated with it are helpful in identifying those who are most prone to developing the disease. In addition, since osteoporosis can be caused or exacerbated by certain diseases or drugs, appropriate steps can be taken to decrease the risk. Everyone has some risk of developing the disease - some more than others. Dr. Robert Heaney of Creighton University at Omaha, Nebraska, says, "Osteoporosis is a total life-style problem." You can't change your physical heredity, but you can change the way you live.

Age
The longer you live, the greater your chances of developing osteoporosis. This is essentially a disease of aging, and all the physiological aspects of growing older contribute to its development. Sluggish, older intestines often don't absorb enough calcium to replenish the bones, and if an adequate amount isn't consumed to begin with, the problem is compounded. Inactive older people often remain inside and frequently do not get enough exercise to maintain bone strength and are not exposed to enough sunshine for the production of Vitamin D.
As the body ages, especially after menopause, there is a decline in the secretion of calcitonin, which discourages bone resorption. To compound the problem, there is an increased production of PTH (parathyroid hormone), which encourages the tearing down of bone tissue. Some research indicates that the aging osteoblasts simply can't manufacture enough new bone for the helpful osteocytes to keep up. As osteocytes die, there are fewer new ones to replace them, which has an adverse effect upon bone replacement. This form of osteoporosis is characterized by a thinning of the bones, which happens slowly over the years without any outward sign. In many cases a bone fracture is the first clue that a woman has this condition. But by this time, osteoporosis has already caused irreversible damage. Loss of the spongy trabecular bone is paramount, and results in many crushing vertebral fractures, primarily in women between 55 and 75 years of age.

Sex
Women with their smaller, thinner bones are far more susceptible to osteoporosis than men. Their peak bone mass is 30 percent less than that of men so there is simply less bone to lose. Women begin to give up bone earlier, and the reduction goes at a much more rapid pace than in men. The calcitonin levels are lower in women so bone destruction is not as effectively controlled. In the early to mid 30's, bones stop growing and start weakening as they give up calcium to the blood. Men lose bone at a constant rate, about 0.3 percent a year for the cortical bone; a slightly higher amount of trabecular bone is destroyed. Women lose about one percent of their trabecular bone and one percent of the cortical bone mass yearly, and that rate accelerates dramatically after menopause. Three to seven years following menopause, the bone loss in women averages three percent. However, as much as eight percent can be lost from the lumbar vertebrae, which are composed mainly of trabecular bone. The formation of new bone can't keep up with the speed at which it's being torn down and there is a great deterioration of bone mass. In approximately 20 years following menopause, the bones in a female skeleton may be reduced as much as 30 percent.
All evidence points to the fact that over a woman's lifetime, estrogen protects bone mass while retarding the rate of loss. The longer and greater the exposure a woman has to estrogen, the lower her risk of osteoporosis. From puberty to menopause estrogen levels are high, and they rise during pregnancy or when oral contraceptives are used. When production dramatically drops as with natural or surgical menopause, the sudden decline in estrogen level affects the complex relationship among other hormones and bone resorption and replacement. Pre-menopausal, amenorrheic women are also at a greater risk for osteoporosis, because their hormone level is already low and menopause often begins early. The longer a woman lives after menopause, the greater the risk of osteoporosis.

Race
Petite, fair skinned Caucasian and Asian women are at a much greater risk of developing the disease. In general, blacks have thicker bones and average ten percent more bone mass than others. Some researchers speculate that skin pigmentation and the higher ultraviolet levels in the tropics stimulate the production of Vitamin D in the skin, which influences bone tissue production. Osteoporosis is much less prevalent among blacks worldwide, and in women of the Mediterranean regions. Others cite osteoporosis as a disease of the privileged, which is more likely to develop in the affluent society of Europe, Scandinavia or North America than in the Third World. The Bantu tribe of South Africa, whose members are hardly the best fed or healthiest people in the world, had the lowest recorded incidence of hip fractures in a 1980 study that also evaluated people in Sweden, the United States, Yugoslavia, and Great Britain. No one really knows why the poor are relatively free of osteoporosis while their better-fed sisters break their bones "right and left." Dr. Diane Meier, Co-Director of the Osteoporosis and Metabolic Bone Disease Program at Mt. Sinai Medical Center, has investigated this contradiction. She conducted a study of 150 black women and 150 white women, aged 25 to 65, to determine whether whites do have an inherent predisposition to excessive bone loss or if body composition and nutritional habits are the key to bone mass. She says, "Blacks, at least in the Northern American population, tend to higher obesity rates and obesity is a protection against bone loss." Dr. Meier's theory is that extra weight stimulates formation of bone because of the increased load placed upon the skeleton. Another factor is the ability of fat tissue to metabolize androgens, a type of hormone which helps protect bone mass.

Family History
"Take a good look at your mother and grandmother to see what's in store for you." Women with a family history of osteoporosis are much more likely to develop this disease. Potential bone mass is a genetically determined factor. A tendency toward early menopause may also be inherited, bringing additional years for the bones to go without estrogen protection.
Progress in the study of the genetics of osteoporosis has been slow. Fractures in individuals are uncommon, making the feasibility of detecting associations between fractures and candidate genes quite unlikely. Bone mineral density (BMD) is a predictor of fracture, but association studies with candidate genes, including those for vitamin D, estrogen, and androgen receptors, have produced inconsistent and contradictory results to date. BMD is too crude a measure to detect variations in remodeling due to genetic differences. Some promising research has indicated, however, that a particular polymorphism of the androgen receptor may serve as a molecular marker of risk for osteoporosis in men.

Health Problems Contributing to Osteoporosis
One out of three men, and one out of five women, who sought medical care for osteoporosis (which was first manifested as a fracture), were discovered to have an underlying illness that contributed to the development of the disease. Diagnosis and treatment of the underlying ailment is essential for appropriate care. Medical conditions that may contribute to the development of osteoporosis include:

Hyperthyroidism (excessive amounts of thyroid hormone): The disease may be due to an overactive thyroid gland or may be the result of taking too high a dosage or too lengthy a regimen of the thyroid hormone in tablet form. The longer it continues, the more severe the bone damage. This condition escalates bone loss and after several years, can cause osteoporosis.

Hyperparathyroidism: Overactivity of the parathyroid gland causes so much hormone to be secreted that it keeps a persistently high level of blood calcium. There is often wasting of bone tissue, as well as abdominal pain, mental dysfunction, and development of kidney stones. Sometimes called the "Hungry Bone Syndrome," this disorder is more common than realized, and mild forms are often discovered in routine lab tests. Since it may not cause symptoms, the silent bone loss in postmenopausal women can be severe. The only treatment is surgical removal of the parathyroid glands.

Cushings Syndrome: This is a disorder in which an overactive pituitary gland stimulates the adrenal glands to produce too much cortisone. One of the effects is osteoporosis. A ‘buffalo hump' develops between the shoulder blades due to a fat pad, and often the spine is bent forward by deformities caused by compressed vertebrae.

Rheumatoid Arthritis: Rheumatoid arthritis is often characterized by a bone calcium content that is 10 percent lower than normal. However, there are thick calcium deposits along the edges of bone and around the joints. Some believe the decrease in bone calcium results from the decreased mobility associated with the disease; however, a similar decrease is not seen in patients with osteoarthritis, which can also cause significant reductions in mobility. Cortical bone in most osteoarthritic patients is tough and hard, while that of an osteoporotic patient is often honeycomb. Those who suffer from rheumatoid arthritis have severe pain, decreased physical activity, and poor appetite and nutrition. Treatment with cortisone aggravates calcium loss and bone weakness. Anti-inflammatory medications often must be taken with antacids, which, in turn, block calcium absorption.

Cancer: Cancerous plasma cells produce a chemical osteoclast activating factor, OAF, which is a powerful stimulator of the production of bone-dissolving osteoclasts. Patients with multiple myeloma often have severe osteoporosis, and several other types of carcinoma show a particular affinity for bones. Chemotherapy for the treatment of breast cancer has been shown to decrease estrogen production by the ovaries, resulting in greater than expected bone loss in treated women.

High Blood Pressure: A study of risk factors for bone loss and related fractures among 3500 elderly women suggested that high blood pressure that is not adequately controlled may increase the risk of osteoporosis. The study, reported in Lancet, suggests that high blood pressure may be associated with abnormal calcium metabolism and bone loss.

Depression: In a review of published research, NIMH-funded scientists reported a strong association between depression and osteoporosis. The literature suggests that depression may be a significant risk factor for osteoporosis. Low bone mineral density (BMD), a major risk factor for fracture, is more common in depressed people than in the general population. Although its causes are unclear, major depression is associated with hormonal abnormalities that can lead to changes in tissue, such as bone. Research suggests that higher cortisol levels, often found in depressed patients, may contribute to bone loss and changes in body composition.
In one study, evidence revealed that bone density at the lumbar spine was 15% lower in 80 men and women older than 40 with major depression compared to 57 men and women who were not depressed. Factors such as smoking, a history of excessive or inadequate exercise, or estrogen treatment did not affect the study, implying that depression per se had an effect on bone mass. The association between depression, BMD, falls, and risk of fracture was also examined in a study of 7,414 elderly women. Depression prevalence was 6%. Depressed women were more likely to fall (70% versus 59%) and had more vertebral (11% versus 5%) and non-vertebral (28% versus 21%) fractures compared with controls. This research underlines depression as a risk factor for osteoporotic fractures, and its identification would improve diagnosis and treatment. When one or more other risk factors is present, such as low BMD, family history, previous fracture, thinness, or smoking, a clinical evaluation for osteoporosis is recommended.
The National Institute of Mental Health (NIMH) has launched a new study of women ages 21 to 45 who are suffering from major depression to find out whether low bone mass is related to depression or stress hormones, such as cortisol. During a 12-month period, researchers will monitor bone loss and the effects of depression and stress on physical health. The study will determine whether women with major depression and normal BMD lose bone mass faster than women without depression, and if the drug alendronate (Fosamax) can maintain or increase bone mass in premenopausal women with major depression and low bone mass.

Other Diseases: Patients with pancreatitis, severe liver disease, and emphysema often suffer from osteoporosis; since 1948, diabetes has also been recognized as a risk factor. Some researchers believe there is a common genetic risk factor for both diabetes and osteoporosis. A gastrectomy often results in poor absorption of calcium, but supplemental Vitamin D and calcium usually resolve the problem. Those with an untreated GI malabsorption syndrome or pancreatitis may develop magnesium deficiency, which results in lower blood levels of calcium and leaching of calcium from the bones.

Prescribed Medications
Many medications contribute to osteoporosis when they are prescribed for other conditions. In the U.S., the population over 65 years of age takes 25 percent of all medications, some of which might have begun early in life to deplete the bones of calcium. The following medications have an adverse effect upon bone health.

Glucocorticoids: Long-term glucocorticoid use is the most frequent cause of drug-induced osteoporosis, and the third leading cause of all osteoporosis in adults. Approximately 90% of long-term users may lose significant amounts of bone, resulting in an increased risk for fracture. Although the mechanism of this effect has not been finally determined, it is believed that glucocorticoids accelerate bone loss in several ways. Decreased bone formation has been demonstrated, with an increase in osteoblast and osteocyte apoptosis. Glucocorticoid use has also been associated with decreased absorption of calcium in the intestine, and lowered activity of the sex hormones. Finally, long-term uses may also contribute to muscle atrophy and progressive loss of muscle strength. All of these factors affect bone formation and may thus over time increase fracture risk. Risk appears to be greatest for fractures of trabecular bone.
Oral forms of these steroids include: Aristocort®, Celestone®, Deltasone®, Decadron®, Medrol®, Prednisone®, Hydrocortisone®, Cortef® and Cortisone Acetate®.
A marked decrease in bone mineral density is typically observed within a few weeks of initiation of treatment in adults, but bone loss will continue even after many years of use. Particular concerns have been raised by the increase in both long-term and intermittent use of glucocorticoids for the treatment of a variety of childhood inflammatory diseases. Current research focuses on the relative effects of inhaled versus oral glucocorticoid use, and the possible benefits of prophylaxis for prevention of fractures.

Antacids: Those that contain aluminum interfere with calcium metabolism; these include: ALternaGEL®, Aludrox®, Amphojel®, Basaljel®, Camalox®, Delcid®, Di-gel®, Gaviscon®, Gelusil®, Kolantyl®, Maalox®, Mylanta®, Riopan®, Rolaids®, Silain Gel® and Simeco®.
The following antacids and medications for ulcer symptoms do not contain aluminum and are thus safer for long term use: Alka Seltzer®, Alkets®, Bi Sodol®, Citrocarbonate®, Lo-Sal®, Mylicon®, Titralac®, Tums®, Tagamet® and Zantac®.

Diuretics: These medications increase calcium loss in the urine, and the thiazides are the most commonly prescribed:Diuril®, Dyazide®, Corzide®, Diamox®, HydroDIURIL®, Aldoril®, Aldoclor®, Hydropres®, Aldactazide®, Apresazide®, Aldoclor®, Hydropres®, Naturetin®. Lasix® has the same effect.

Tetracyclines: These drugs bind to calcium and impair its absorption. The medications should be taken two to three hours apart from calcium supplements or calcium rich food. Individuals who take these medications often have high levels of calcium in their urine, but long lasting harm has not been proven.

Anticonvulsants: Dilantin, phenobarbital, Primidone® and Phensuximide® all may interfere with Vitamin D metabolism in the liver and decrease calcium absorption. Anyone on these medications may need calcium and Vitamin D supplements.

Miscellaneous Medications: Some of these drugs adversely affect bone health by encouraging the withdrawal of calcium from the bones or by interfering with Vitamin D production:

• antituberculars including Isoniazid®, Seromycin®, Capastat®
• anticancer agents such as Dactinomycin (Cosmegen)
• Questran® to lower cholesterol levels
• Benemid® and ColBENEMID® for gout
• Doriden® and lithium

Accutane® mobilizes calcium and supplements should be taken with long-term use.
Long-acting benzodiazepines and sedatives have also been implicated in the development of osteoporosis.It would be wise for any patient to consult the prescribing physician as to the effect of his or her medications upon calcium nutrition, because many helpful and frequently prescribed medications can have harmful side effects on bone health.

Life Style Factors
In addition to the risk factors listed above, there are a variety of lifestyle characteristics that have also been shown to increase the risk for development of osteoporosis and subsequent bone fracture. These include nutritional status, smoking and excessive alcohol use, and exercise and general activity level. Because modification of these factors is one of the most important strategies for osteoporosis treatment and prevention, they will be covered in depth in those sections of this course.

THE OSTEOPOROSIS SCREENING ACT OF 2001(HR 1720 & SB 826)

Bone mineral density (BMD) tests or bone mass measurement (BMM) tests can measure bone density in various sites of the body. A bone mineral density test can detect osteoporosis before a fracture occurs. They are also good indicators of possible future fractures; they help determine the rate of bone loss and monitor the effects of treatment.
Many Medicare beneficiaries at risk for osteoporosis are not receiving BMD tests due to the requirement of a 20 percent co-payment, which can range from $5 to nearly $30. Studies show that patient cost sharing in general deters people from seeking medical services. These deterrent effects are greatest for low-income individuals, especially those in poor health, and for preventive services. Higher income seniors may also lack the motivation to pay for diagnosis of "silent" (asymptomatic) diseases.
The Improved Access to Osteoporosis Testing Act of 2001, introduced by Sen. Blanche Lincoln (D-AR) and Rep. John Lewis (D-GA-5), proposes to eliminate Medicare cost sharing for bone mass measurement, thus providing millions of women with affordable access to a test that could help prevent fractures that may cause costly hospitalization and nursing home admissions. The goal is to make bone mass measurement screening a routine and accessible part of a woman's total health program.

Diagnosis of Osteoporosis

In osteoporosis, two factors are important: the amount of tissue inside the bone itself and the quality and health of the tissue. Ordinary X-rays can show fractures typical of osteoporosis, but they are not helpful in determining the amount of bone mass. A person would have to lose as much as 40 percent of his bone calcium before it would become obvious on an X-ray. Therefore, techniques have been developed to measure the bone mass in the arms, legs and spine. They are helpful both in determining the degree of damage and in monitoring treatment response.
At the present time, the clinical diagnosis of osteoporosis is made by measurement of bone mineral density (BMD) with a technique called dual x-ray absorptiometry (DXA). A very tiny beam of particles emitted by a radioactive isotope of iodine is projected through the bones of the forearm, hip or spine. An instrument called an absorptiometer measures the number of particles that can be projected through the bone. The technology uses miniscule doses of radiation, approximately one-fifth that received from a standard chest x-ray for example, and provides fast, accurate, painless and completely reproducible results.
BMD as measured by this technique is expressed as an absolute value and may be designated as either the number of standard deviations from the mean of age matched controls (Z score), or the number of standard deviations from the young normal mean (T score). The World Health Organization currently defines osteoporosis as a BMD of 2.5 or greater standard deviations below the mean value for young adults. Efforts are currently underway to develop a more flexible set of diagnostic criteria, which would also include other measures of risk such as bone turnover markers or evidence of a previous fracture.
In 1998 the Food and Drug Administration (FDA) approved a new device for rapid screening for osteoporosis. The device, called the Sahara Clinical Bone Sonometer, transmits sound waves through the heel of the foot to measure bone density. The sonometer is a portable, inexpensive device that may make screening more accessible. Although it is accurate enough for screening, it's not currently as sensitive a diagnostic tool as DXA.
The use of biochemical markers of bone turnover in the management of osteoporosis raises considerable interest. A battery of biochemical markers are now available that allow for assessment of the rate of bone formation and bone resorption of the skeleton. These markers appear to be useful for the individual monitoring of osteoporotic patients treated with antiresorptive drugs, especially for those agents that induce only a small increase in BMD. Such markers can also be useful in selected cases to improve the assessment of the individual risk of fractures when BMD measurement by itself does not provide a clear answer. Prospective studies have shown that urinary or serum levels of markers above the premenopausal range are associated with a 2-fold increase in the risk of fragility fractures, independent of the level of BMD. The combined use of BMD and bone markers is likely to improve the assessment of the risk of fractures in those cases.
A history of a low-trauma fracture, or a fracture sustained after the age of 50, is one of the strongest and most consistent risk factors for subsequent fracture; for hip and vertebral fractures, for example, the increased risk is independent of BMD. A history of fracture should be included in clinical guidelines to identify patients in whom a BMD test should be performed and for whom treatments are most likely to be beneficial. Without proper followup, fractures represent a missed opportunity for appropriate intervention.

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