Normal Anatomy & Physiology of Bone 

Behavioral Objectives 

Certifications 

TYPES OF OSTEOPOROSIS 
Risk Factors and Pathophysiology 

Postmenopausal Osteoporosis 

Senile Osteoporosis 

Secondary Osteoporosis 

CLINICAL MANIFESTATIONS AND COMPLICATIONS 
Diagnosis

TREATMENT AND PREVENTION 
Vitamin D and Calcium 

Biophosphonates

HRT

Selective Estrogen Receptor Modulators 

Calcitonin 

Other Therapies

CASE STUDY 

ROLE OF THE PHARMACIST

REFERENCES 

FIGURES 
Figure 1

Figure 2

Figure 3

Figure 4

Figure 5

Figure 6 

Photo

Helping the Patient Prevent and Treat Osteoporosis

Malachia C. Clark, PharmD Candidate and Harold J. Bruyere, PhD

Ms. Clark is a PharmD Candidate at the University of Wyoming. Dr. Bruyere is Professor of Pathology and Toxicology at the University of Wyoming School of Pharmacy in Laramie, WY. 

Introduction 

Definition, Prevalence, and Significance

Osteoporosis is the term used for all those diseases characterized by a significant reduction in the mass of normal bone per unit volume^1,2 (Figure 1) that ultimately result in more fragile bone and fractures. In this disorder, the rate of bone resorption (breakdown) is greater than the rate of new bone formation. Bone mineralization is normal in contrast with the bone disease osteomalacia in which mineralization is poor. Osteoporosis can be generalized (involving major portions of the skeleton) or localized (involving one or, at most, several segments of the skeleton) as may occur with immobilization of a limb as a result of a fracture.

An estimated 25 million Americans are affected by osteoporosis, approximately 14 million of whom are women. Women are more susceptible to osteoporosis than men because of their lower peak bone mass, loss of ovarian function, and reduced estrogen synthesis following menopause. Overall, approximately 85% of women develop some degree of osteoporosis during their lifetime. This includes more than half of all women over the age of 45 and 90% of females over age 75.³ 

Complications of the disorder, especially hip fractures, make osteoporosis the twelfth leading cause of death in the United States. Death often results from respiratory complications secondary to immobility^.4 Hip fractures, by far the most serious complication, are associated with a mortality rate of up to 33% during the 2 years that follow⁵; and up to one half of hip fracture patients are unable to walk independently again after the fracture heals.^6,7 The incidence of specific fractures increases with decreasing bone density.^8,9 However, low bone density at one site does not necessarily imply fracture risk at other sites, and the course of the disease is often unpredictable. 

Osteoporosis is a major and growing public health problem, especially because the elderly population is increasing. The total annual cost of osteoporosis in the United States has been estimated at more than $7 billion.¹⁰ Although once considered an inevitable consequence of aging, today osteoporosis is a preventable and treatable disorder.

In this article, the authors will:

Normal Anatomy and Physiology of Bone

There are two basic types of bone: cortical and trabecular. Cortical bone is dense and compact, has four times the mass of trabecular bone, and constitutes about 80% of adult bone.^6,11 Trabecular bone has a honeycomb-like appearance and is the more metabolically active of the two types of bone.¹¹ Only about 20% of adult bone is trabecular bone. Trabecular and cortical bone are made up of three components. These components include the protein matrix, mineralized bone, and bone cells. The protein matrix gives bone its flexibility and consists of type I collagen fibers and proteoglycans. Minerals, calcium, phosphate, magnesium, sodium, and carbonate are stored in mineralized bone, which is the source of the compressional strength of bone. Bone cells, osteoclasts and osteoblasts, are largely responsible for bone mineral homeostasis and maintaining bone mass. The bone cells make up only about 3% of the total bone mass.⁶

Figure 1.  Scanning of Electron Micrographs of Normal (left) and Osteoporotic (right) Vertebral Trabecular Bone.¹¹ 

There are four types of bone structure: long, short, flat, and irregular. Long bones consist of a long shaft, the diaphysis, and a broad end, the epiphysis (Figure 2). Short bones are cuboidal in shape and include bones found in the wrists and ankles.¹² The ribs represent an example of flat bones, and irregular bones include vertebrae, pelvic bones, and various facial bones.^6,12 Cortical bone is found primarily in the diaphysis of long bones, surrounding the bone marrow.¹³ Short, flat, and irregular bones, as well as the epiphysis of long bones, are surrounded by a thin layer of cortical bone but are composed primarily of trabecular bone.^6,12,13

Figure 2.  Diagram Demonstrating the Structure and Composition of a Typical Long Bone.⁶⁹

Osteoclasts are bone-resorbing cells.¹⁴ Osteoclasts dissolve bone, creating cavities and releasing minerals into the serum.⁶ Osteoblasts are bone-forming cells.¹⁴ Osteoblasts synthesize bone-utilizing serum minerals to fill in the bone cavities created by osteoclasts. Normally, osteoclasts and osteoblasts work in concert. The amount of bone resorbed by osteoclasts equals the amount of bone formed by osteoblasts, thus maintaining skeletal bone mass.⁶ 

The resorption and formation of bone by osteoclasts and osteoblasts is termed bone remodeling. In a normal healthy adult, one bone remodeling cycle takes about 4 months to complete.^6,14 About 3% of cortical bone and 25% of trabecular bone is remodeled each year.⁶ 

Parathyroid hormone (PTH), vitamin D, and calcitonin play major roles in bone remodeling and maintaining bone mass. When serum calcium levels are low, the secretion of PTH from the parathyroid gland is increased.¹⁴ PTH increases serum calcium via three physiologic mechanisms: the hormone stimulates osteoclasts to break down bone and liberate stored calcium; PTH facilitates the metabolization/conversion of vitamin D to its active form, 1,25-dihydroxyvitamin D, in the kidneys, and PTH causes reabsorption of calcium from the kidneys (Figure 3). 1,25-dihydroxyvitamin D acts with PTH to increase serum levels of calcium. Like PTH, 1,25-dihydroxyvitamin D activates osteoclasts resulting in increased bone resorption and increases reabsorption of calcium from the kidneys. 1,25-dihydroxyvitamin D also promotes absorption of calcium from the gastrointestinal tract.⁶ With increased concentrations of calcium in the serum, secretion of PTH is suppressed and metabolization of vitamin D is decreased. Once serum calcium levels are raised above 12 mg/dL, calcitonin is secreted from the thyroid gland. Calcitonin decreases serum calcium levels by activating osteoblasts. The activated osteoblasts increase bone formation, removing calcium from the serum.¹⁴ In a healthy adult, PTH and calcitonin indirectly regulate one another, maintaining both serum calcium levels and skeleton bone mass.

Figure 3.  Flowchart Showing Normal Physiologic Mechanisms for Maintaining Serum Calcium Concentrations in the Human Body. (Parathyroid hormone, calcitonin, and 1,25-dihydroxyvitamin D play important roles.)

Types of Osteoporosis

Osteoporosis is not a single disease state with one cause, but rather a very heterogeneous disease process with a wide variety of contributing factors.¹⁵ Three basic types of osteoporosis have been established: postmenopausal, senile, and secondary.⁶ The types are not distinct, however, because risk factors overlap.

Postmenopausal osteoporosis (type I) is the classic form of the disease and was initially described in 1941.¹⁶ This type of osteoporosis affects primarily trabecular bone (Figure 2) as early as 5 years after menopause. There is minimal cortical bone loss associated with type I osteoporosis. Since the rate of trabecular bone loss is threefold the premenopausal rate, weight-bearing bones are primarily affected. The types of fractures that are most commonly associated are those of the vertebrae, ankle, and distal radius.^17-22

Senile (age-related) osteoporosis (type II) affects men and women typically after age 70 but may begin as early as age 35.²³ With type II disease, there is significant loss of both trabecular and cortical bone. Consequently, hip and multiple wedge vertebral fractures are the most common types of fractures,²³ although fractures of the humerus, tibia, and pelvis are also common.

Secondary osteoporosis (type III) may occur at any age in both genders and can be attributed to immobilization, medications, and/ or other disease states. Both trabecular and cortical bone loss is significant. Spine and hip fractures are associated with type III disease.

Risk Factors and Pathophysiology

A major pathophysiologic mechanism in the development of osteoporosis is an imbalance between the rates of bone resorption and formation. Factors that either cause acceleration of resorption or retardation of new bone production predispose to brittle and easily fractured bone.

Postmenopausal Osteoporosis 

Bone loss proceeds rapidly after menopause.² A deficiency in circulating estrogen concentration is clearly associated with an increase in osteoclast-mediated bone resorption. Estrogen deficiency promotes the release of the cytokines interleukin-1 (IL-1)^24,25 and tumor necrosis factor alpha (TNF-a)²⁵ from blood monocytes (Figure 4). Both are known to promote bone resorption.²⁶ Estrogen replacement decreases cytokine production.^26,27 The estrogen-mediated increase in bone resorption leads to decreased parathyroid hormone secretion,^17,28,29 which, in turn, leads to decreased production of 1,25-dihydroxyvitamin D^30,31 and increased renal calcium excretion.²⁶ Decreased circulating serum 1,25-dihydroxyvitamin D causes impaired calcium absorption,³⁰ which may further increase bone loss.³²

Figure 4.  Flowchart Showing Pathophysiologic Mechanisms Involved in the Development of Postmenopausal Osteoporosis.

Senile Osteoporosis 

The threshold for fractures from bone loss is reached much sooner in women than men, primarily because women generally have less peak bone mass and suffer accelerated bone loss with estrogen deficiency. During the premenopausal period, trabecular bone loss proceeds at a rate of 3% per decade but triples to 9% after menopause.³³ The incidence of osteoporosis in men is not as high as for women,³⁴ since, over a lifetime, women lose about one third of their trabecular bone and men lose only about one fourth.³⁵

Four factors contribute significantly to age-related osteoporosis: decreased osteoblast function (and, consequently, decreased new bone formation), decreased calcium and vitamin D absorption, biochemical imbalances, and sex hormone deficiencies. After age 40, less bone is produced than is resorbed³⁶ and this imbalance increases with aging. This does not result from a complete lack of osteoblast function, however, because fracture repair in the elderly is not delayed. Impairment in the regulation of osteoblast function may be the result of both systemic and local abnormalities. For example, calcium absorption decreases with age in both genders, especially after age 70. This may, at least in part, be caused by an age-related decrease in the ability of 1,25-dihydroxyvitamin D to promote intestinal absorption of calcium.^37,38 Furthermore, many elderly consume less than the recommended daily requirements of both calcium and vitamin D. Minimal exposure to sunlight (and, therefore, decreased skin metabolism) and impaired renal metabolism of vitamin D to active metabolites of the vitamin may also play a role in enhanced bone loss by lowering serum 1,25-dihydroxy-vitamin D levels.^37,39,40 Serum parathyroid hormone concentrations are increased secondary to decreased serum calcium and promote bone loss by activating osteoclast activity (Figure 5). Gradually decreasing serum concentrations of testosterone contribute to the development of osteoporosis in the aging male.⁴¹

Figure 5.  Flowchart Showing Pathophysiologic Mechanisms Involved in the Development of Age-Related Osteoporosis.

Secondary Osteoporosis 

The anticoagulant heparin, glucocorticoids (eg, prednisone), synthetic thyroid hormone, anticonvulsants, and cyclosporine are examples of medications that have been established to cause bone loss and fractures. Although the mechanism is unknown, more than 15,000 units of heparin per day for more than 3 months causes significant osteoporosis in pregnant women. Approximately one third of pregnant women showed a bone loss in the proximal femur of more than 10%.⁴² Osteoporosis caused by heparin therapy usually resolves when the drug is discontinued.

Synthetic thyroid hormone is known to increase the number of osteoclasts, lower serum calcitonin, and promote bone resorption. Doses greater than 200 mcg/day or at least 1.6 µg/kg have been associated with bone loss. Thyroid hormone users who are also taking synthetic estrogens, however, suffer less bone loss.⁴³

Anticonvulsants increase metabolism of vitamin D and can cause osteoporosis when taken long term. Transplant patients are at risk for developing osteoporosis from long-term glucocorticoid and/or cyclosporine therapy to prevent rejection⁴⁴ as are patients who take glucocorticoids for any indication.⁴⁵ Glucocorticoid-induced osteoporosis appears to be related to a decreased rate of bone formation, an increased rate of bone resorption, and a vitamin D–independent inhibition of intestinal calcium absorption.¹ Glucocorticoid use is a powerful risk factor for predominantly vertebral fractures in both men and women.²³ 

Other factors that significantly increase the risk for developing osteoporosis are genetic predisposition, lifestyle, medical disorders, and prolonged bed rest.⁶ Certain races are at higher risk (Caucasians and Asians), and the disease is associated with both a positive family history and a small body frame.

Smoking, as well as excessive use of alcohol, caffeine, aluminum-containing antacids, and a lack of physical activity are lifestyle choices that promote osteoporosis. Smoking lowers bone mass and increases fracture rates, at least in part, by increasing the metabolism of sex hormones.^46-48 Excessive use of alcohol may induce nutritional deficiencies in calcium and vitamin D.⁶ Caffeine and aluminum-containing antacids increase urinary calcium excretion.⁶ High-intensity strength training programs,⁴⁹ regular walks,⁵⁰ swimming,⁵¹ and other forms of regular physical exercise have been shown to prevent bone loss.

Examples of disease states which, independent of therapy, can cause osteoporosis include the following: hyperthyroid disease characterized by elevated serum levels of natural thyroid hormone and increased urinary calcium excretion; hyperparathyroid disease associated with increased blood parathyroid hormone concentrations; and Cushing’s syndrome in which natural glucocorticoid levels are high. Some gastrointestinal disorders (e.g., obstructive jaundice) are associated with both calcium malabsorption and deficiency and promote osteoporosis. Finally, prolonged bed rest promotes osteoporosis by increasing the activity of osteoclasts.

Clinical Manifestations and Complications

The symptoms of osteoporosis are often episodic and totally unrelated to the severity of the disease state.⁶ When pain occurs, it is related to a fracture and can be chronic in nature. However, the typical clinical presentation of the patient with osteoporosis is that of shortened stature (because of collapse of vertebrae); kyphosis (increased convexity in the curvature of the thoracic spine as viewed from the side); lordosis (an abnormal concavity of the lumbar spine as viewed from the side); and/or a fracture, most commonly of the vertebrae, hip, or forearm (Figure 6). Fractures frequently occur with minimal trauma and can be caused by bending, lifting, or falling. Vertebral body collapse is the most frequently seen fracture associated with osteoporosis, especially in early postmenopausal women.⁶ As a result, acute back pain of variable intensity occurs and radiates around the flank into the abdomen, but usually resolves within 2 to 3 months. Some patients may present with a fracture upon X-ray but without pain. Acute pain may occasionally be followed by chronic pain, described as nagging, deep, dull, localized to the fracture region, and brought about by sudden changes in position (e.g., turning in bed). Chest wall abnormalities can lead to respiratory problems. The presence of systemic symptoms, such as weakness or weight loss, suggests that osteoporosis is caused by an underlying disease.⁵²

Figure 6.  Diagrams Showing Two Common Complications 
of Osteoporosis, Kyphosis, and Lordosis.⁷⁰

Diagnosis

All patients who present with risk factors and/or early signs of osteoporosis should undergo a comprehensive medical evaluation to exclude secondary causes, to assess the extent of bone loss and fractures, and to provide baseline measurements to evaluate the effectiveness of treatment.⁵²

A thorough medical history should be taken. The history should include the chronology and location of any fractures, time course and characteristics of pain, previous treatments, age at onset and type of menopause (i.e., natural or surgical), family history of osteoporosis, level of physical activity, use of tobacco or alcohol by the patient, and the presence of other risk factors.⁵²

Physical examination should include careful measurement of height and a search for findings suggestive of systemic disease. All patients should have a complete blood cell count and serum chemistry panel, determination of erythrocyte sedimentation rate, and urinalysis. Serum 1,25-hydroxyvitamin D should be measured when osteoporosis may be caused by gastrointestinal disease or a vitamin D deficiency. Measurement of serum 1,25-dihydroxyvitamin D has been shown to be of little value, however, in the diagnosis of osteoporosis.⁵² Standard X-rays of both the thoracic and lumbar spine should be obtained to evaluate the severity of the disease and to provide a baseline for assessing the effect of therapy.

The advent of reliable methods for assessing bone density has revolutionized the evaluation of patients for osteoporosis. Bone densitometry has now been demonstrated to predict the risk of a subsequent fracture⁵³ and, although somewhat controversial, can be useful in assessing response to treatment. The most appropriate sites to assess bone density are the lumbar spine and neck of the femur. Both sites should be evaluated. Dual energy X-ray absorptiometry (DEXA) has almost completely supplanted other techniques for assessing bone density and represents the single most beneficial procedure for diagnosing osteoporosis. DEXA can detect losses as minimal as 1%, represents a relatively inexpensive screening tool, and delivers negligible radiation.

Biochemical markers to assess bone turnover have only recently become widely used. Although results can be highly variable, these tests have major implications for therapy, because patients with high bone turnover respond well to estrogen⁵⁴ and calcitonin,⁵⁵ whereas patients with low bone turnover are unlikely to have a significant therapeutic response.⁵³ Measurement of two urinary pyridium crosslinks provides a reliable and sensitive method for assessing bone turnover. Deoxypyridium is more specific, but pyridium is easier to detect because it is present in higher concentrations.

In patients who appear to be ill and/or have systemic symptoms, a bone marrow aspirate should be considered to rule out cancer.⁵²

Treatment and Prevention

Prevention is the optimal goal in treating osteoporosis since there is no cure for the disease. Prevention should begin in childhood. Several lifestyle modifications have been recognized that aid in the prevention of osteoporosis. Maintaining an adequate daily intake of calcium and vitamin D is one of these modifications.^6,56-58 Sufficient amounts of calcium and vitamin D can be acquired through diet, supplements if necessary, and sunlight in the case of vitamin D. Vitamin D requirements may be met with as little as 5 to 20 minutes of direct sunlight, two to three times per week.⁶

Limiting alcohol and caffeine use,^6,58 discontinuing smoking, and increasing physical activity are also helpful in preventing osteoporosis.^6,56-58 Weight-bearing exercise, such as running, walking, and aerobics, can increase bone mass density and improve balance.^6,58 Improved strength and balance also decrease the risk of falls, preventing fractures.⁶ Avoiding sedating drugs is also helpful in the prevention of falls and fractures in geriatric patients.⁵⁷

In addition to lifestyle modifications, pharmacologic agents can be used to treat and prevent osteoporosis. These include calcium and vitamin D supplements, hormone replacement therapy (HRT), the bisphosphonates, raloxifene, and calcitonin. Past and present medical conditions, current medications, patient lifestyle, patient preference, and cost should be taken into account when selecting appropriate therapy.⁵⁸ 

Calcium and Vitamin D 

Calcium and vitamin D supplements may increase bone mass density and decrease fractures, especially in certain patient populations.^6,57,58 Patients not receiving the recommended daily allowances (RDAs) of calcium and vitamin D from their diet,^6,58 nursing home residents,⁵⁹ and patients on prevention and treatment regimens for osteoporosis should take these supplements daily^.6,59 Calcium and vitamin D supplements should not be used alone to prevent osteoporosis.⁶

The RDA of calcium varies. In general, men and women older than 65 years of age and postmenopausal women not on HRT should receive 1,500 mg of calcium per day. Men and women older than 19 years of age and postmenopausal women on HRT should receive at least 1,000 mg of calcium per day.^6,56,58

There are two major types of calcium products, calcium carbonate and calcium citrate. Calcium carbonate has a higher calcium concentration per tablet and is less expensive than calcium citrate. However, the absorption of calcium carbonate depends on acid production in the gastrointestinal tract. This supplement must be taken with meals for optimal absorption. Some patients produce less stomach acid with age, inhibiting the absorption of calcium carbonate. Calcium citrate is an effective supplement for these patients, and the supplement may be taken on an empty stomach.⁶

The optimal dose of vitamin D is unknown.⁵⁸ Currently, the RDA is 200 IU/day for those younger than 50 years of age, 400 IU/day for those older than 50 years of age, and 600 IU/day for those older than 70 years of age.⁶ 

Hormone Replacement Therapy 

HRT is considered the most effective preventive approach to osteoporosis in postmenopausal women.^6,56,60 The beneficial effects of HRT are greatest in patients beginning therapy within 5 years of menopause. Patients should remain on HRT for at least 5 years,⁵⁷ but the longer the better. Discontinuation of HRT after any period of use results in bone loss. Some women should not use HRT. Absolute contraindications are active or suspected estrogen-dependent cancer, severe liver disease, abnormal vaginal bleeding, and active vascular thrombosis.⁶

Estrogen receptors are located within cells throughout the body. Estrogen prevents bone loss and fractures by increasing intestinal calcium absorption, inhibiting parathyroid hormone, and decreasing cytokines, calcium renal excretion, and osteoclast activity.⁶ In addition to preventing osteoporosis, benefits of HRT include a decreased risk of cardiovascular disease,^6,56-58,60 control of many of the troublesome symptoms of menopause including hot flashes and mood disturbances,^6,56,57 and the possible prevention of dementia.^6,57,58

There are many potential complications associated with HRT. When estrogen is given alone to a woman with an intact uterus, there is a 12-fold increased risk of endometrial cancer.⁶ However, the administration of progestin cyclically or continuously with estrogen eliminates this risk and may even be protective. 

An association between HRT and breast cancer is controversial. The risk for developing breast cancer as a result of HRT appears to be slight. However, this risk, as well as other complications associated with HRT, should be discussed with all women. Other complications of HRT include the return of menstrual bleeding, breast tenderness, migraine headaches, deep venous thrombosis, and pulmonary embolism.⁵⁷ Common side effects are vaginal spotting and bleeding, breast tenderness and enlargement, pedal edema, and weight gain.⁶ Before initiating therapy with HRT, the benefits and risks for each patient must be carefully weighed.⁵⁶

Bisphosphonates

Bisphosphonates are the treatment of choice for osteoporosis in men,^56,61 patients receiving long-term glucocorticoid therapy,^62,63 and women who are unable or unwilling to undergo HRT.⁶⁰ This class of drugs has been shown to increase bone mass density and decrease the risk of vertebral and hip fractures.^6,56-58,60 Bisphosphonates bind to mineralized bone, preventing the adherence and resorption of bone by osteoclasts. One bisphosphonate, etidronate, has been found to inhibit both osteoclast and osteoblast activity. As a result, etidronate can cause osteomalacia if not given cyclically,^6,58 and alendronate has become the bisphosphonate of choice.⁶

Alendronate is indicated for the treatment and prevention of osteoporosis in postmenopausal women and for treatment of glucocorticoid-induced osteoporosis in men and women.^6,58 The current recommendation is a dose of 5 mg/day for prevention and 10 mg/day for treatment.^6,57,58 The drug must be taken at least 30 minutes before breakfast with water.^6,56-58,61 Other medications, including calcium and vitamin D supplements, should be taken at a different time of day.^6,56 To decrease the risk of esophageal irritation and the formation of esophageal ulcers, the patient should remain in an upright position for at least 30 minutes after taking alendronate.^6,56,57,61 The most common side effects of this drug are nausea and diarrhea.⁶

The standard dosage regimen for etidronate is 400 mg/day for 2 weeks followed by 11 weeks of calcium supplements. This cycle is repeated every 3 months.^6,57,58 Other bisphosphonates under investigation for the treatment of osteoporosis include pamidronate, risedronate, clodronate, ibandronate, and tiludronate.^6,57

Selective Estrogen Receptor Modulators

One selective estrogen receptor modulator (SERM), raloxifene, is considered a useful alternate therapy for women who cannot or are unwilling to take HRT.⁵⁸ SERMs are synthetic drugs that act as estrogen agonists in some tissues and estrogen antagonists in others. Another SERM, tamoxifen, is used to treat and prevent breast cancer.⁶⁴ Tamoxifen is a breast tissue antagonist and a bone and uterine tissue agonist.⁶ The drug has been associated with increased bone density^6,57 but is also associated with an increased risk of endometrial cancer.^6,57,64

Raloxifene is an estrogen agonist in bone and an estrogen antagonist in breast and uterine tissue.^6,64,65 Raloxifene is associated with increased bone mass density^{6,57,58,60,64,65} and recently has been shown to decrease the risk of vertebral fractures in postmenopausal women.^64,65 The effect of raloxifene on increased bone mass density is less than that seen with alendronate, but the decreased risk of vertebral fractures may be comparable.⁶⁵ 

Raloxifene also decreases serum concentrations of total cholesterol and low-density lipoproteins.^6,57,58,60 The protective effect on cardiovascular disease is suspected but unproven.^58,60 Raloxifene does not stimulate endometrial growth and may prevent breast cancer, but the long-term effects of this drug on these cancers are also still unknown.^6,57,64 Women at risk for venous thromboembolic events should not use raloxifene.^6,58,65 The most common side effects of this drug are hot flashes.^6,58 Several other SERMs are under investigation; these include droloxifene, idoxifene, and levormeloxifene.⁵⁷ 

Calcitonin

Calcitonin is less effective than HRT or bisphosphonates in increasing bone mass density and decreasing the risk of fractures.^6,66,67 However, calcitonin has been shown to provide bone pain relief for patients with osteoporotic fractures.^6,56-58 For this reason, the hormone is useful in treating patients with acute fractures or chronic pain associated with osteoporosis.⁶ Calcitonin inhibits osteoclast activity, preventing bone resorption.^56-58 Two dosage forms are available: intranasal spray and subcutaneous injection.^6,57,58 The nasal spray is preferred because it produces fewer side effects and is more convenient to use.^57,58 The standard intranasal dose is 200 IU daily, alternating nares.^6,57,58 Side effects of the nasal spray include nasal congestion and irritation and rhinitis.^6,58

Other Therapies

Testosterone has been shown to be helpful in treating osteoporosis in elderly and hypogonadal men.⁶³ However, the hormone is associated with many side effects, and its use is limited in other patient populations. In some studies, oral contraceptives have been shown to increase bone mass.⁶ However, the benefit of these hormones in the treatment and prevention of osteoporosis needs further investigation. Some promising investigational therapies include fluoride, growth hormones and growth factors, and parathyroid hormone.^6,57,68

Case Study Patient Presentation

Mrs. K is a widowed and frail, 75-year-old Caucasian female who has been living alone and has been housebound for 5 years because of chronic hip and back pain. She is 5 feet 3 inches tall, weighs 105 pounds, and has shown a 2.5-inch height reduction in the past 5 years.  She has a history of fractures, including a right hip fracture and right forearm fracture following a fall and a vertebral fracture following bending to pick up her eyeglasses. She has been a one-pack-a-day cigarette smoker for 35 years and has been diagnosed with chronic bronchitis and emphysema. She also has a previous 4-year history of hyperthyroidism (Graves disease) for which she was treated with oral radioactive iodine and became hypothyroid. She has been taking levothyroxine for her underactive thyroid condition for 18 years. She has a positive family history for fractures (mother and two sisters). She does not use caffeine or alcohol regularly. In addition to her thyroid medication, she is also taking hydrochlorothiazide for hypertension and prednisone for rheumatoid arthritis.

Analysis

Role of the Pharmacist in Preventing and Treating Osteoporosis

Pharmacists can play a significant role in both the prevention and treatment of osteoporosis. A competent pharmacist should be able to identify most patients at risk for the disease through an evaluation of medications, current health problems, lifestyle factors, and age. Once patients with risk factors have been identified, the pharmacist has several options to help decrease the probability that these patients will develop osteoporosis. Pharmacists can provide counseling, emphasizing the importance of prevention through lifestyle modifications. They may also make brochures readily available and can recommend helpful over-the-counter products. For example, some patients find choosing a calcium product confusing. Pharmacists can recommend a daily dose, type of supplement (carbonate or citrate), and calcium carbonate products with good dissolution and disintegration rates. The pharmacist may also emphasize the importance of a thorough physical examination to high-risk individuals not under the care of a physician before serious complications develop.

Pharmacists can also assist with the pharmacologic regimens prescribed for patients. They should provide counseling about the benefits and risks of each drug, as well as about drug interactions and specific administration guidelines. The pharmacist has a very important role in improving patient compliance. Many women take HRT to treat the immediate bothersome effects of menopause, including hot flashes, unaware of the long-term benefits of this therapy. Pharmacists can emphasize these benefits (prevention of fractures, heart attacks, strokes), which may improve compliance among this patient population. Certaom ,edocatopms are particularly inconvenient for patients to take. Assisting patients by organizing medications and supplements into detailed dosing schedules can improve compliance in these individuals. By emphasizing prevention in patients with risk factors and encouraging medication compliance, the pharmacist can improve the long-term health outcomes of many patients.

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Introduction  |  References

Temple University School of Pharmacy is approved by the American Council on Pharmaceutical Education (ACPE) as a provider of continuing pharmaceutical education. Its CE programs are developed in accordance with the “Criteria for Quality and Interpretive Guidelines” of ACPE. This program is acceptable for 2.0 hours of Continuing Education Credits (0.2 CEU) through August 31, 2003. ACPE Pgm I.D.  057-999-00-042-H01.

Acknowledgments

The authors wish to extend their thanks and appreciation to Miss Lyn Batia for developing and preparing the flowcharts in Figures 3, 4, and 5; Joseph F. Steiner, PharmD, Professor of Pharmacy Practice and Director of Pharmacy Practice, University of Wyoming School of Pharmacy, and Melissa Foss, PharmD, Assistant Professor of Pharmacy Practice, University of Wyoming School of Pharmacy, for their thorough critiques of the manuscript; and Loren A. Thompson, RPh, Assistant Lecturer and Professional Experience Coordinator, University of Wyoming School of Pharmacy, for his suggestions relative to the role of the pharmacist in preventing and treating osteoporosis.