PREVENTION AND TREATMENT OF OSTEOPOROSIS
AMANDA MAYER, PharmD
Amanda Mayer is a graduate of the University of Montana, Skaggs School of Pharmacy. She has clinical experience as a pharmacist in the inpatient mental health setting, which is her passion. She has also done fill-in work at retail pharmacies throughout her career. Amanda appreciates the wide variety of professional opportunities available to pharmacists. Amanda loves spending time with her family and spends most of her free time exploring new restaurants, hiking in the summer, snowboarding, and cross-country skiing in the winter.
Osteoporosis is a common bone disease that may lead to an increased risk of fractures due to the weakening of bone tissue, structure, and strength. Osteoporosis affects over 10 million adults in the United States. There is no cure for osteoporosis but there are several FDA-approved medications that can help reduce fracture rates for patients with osteoporosis. Current FDA- approved pharmacologic options include bisphosphonates, estrogen-related therapy, parathyroid hormone analogs, RANK-ligand inhibitor, sclerostin inhibitor, and calcitonin salmon. Calcium and vitamin D are also mainstays of prevention and treatment. Approximately 30-50% of patients do not take their medications correctly. The integrated healthcare team can help educate patients on lifestyle modifications to reduce fall risk and fractures as well as the importance of taking osteoporosis medications to help reduce fracture risk.
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Universal Activity Number (UAN): The ACPE Universal Activity Number assigned to this activity is
Pharmacy Technician 0669-0000-23-074-H01-T
Credits: 2 hours of continuing education credit
Type of Activity: Knowledge
Media: Internet Fee Information: $6.99
Estimated time to complete activity: 2 hours, including Course Test and course evaluation
Release Date: May 16, 2023 Expiration Date: May 16, 2026
Target Audience: This educational activity is for pharmacists.
How to Earn Credit: From May 16, 2023, through May 16, 2026, participants must:
Read the “learning objectives” and “author and planning team disclosures;”
Study the section entitled “educational activity;” and
Complete the Course Test and Evaluation form. The Course Test will be graded automatically. Following successful completion of the Course Test with a score of 70% or higher, a statement of participation will be made available immediately. (No partial credit will be given.)
Credit for this course will be uploaded to CPE Monitor®.
Learning Objectives: Upon completion of this educational activity, participants should be able to:
List the T-score values for patients with normal, low bone mass, and osteoporosis
Identify medication classes that may contribute to or worsen osteoporosis
Explain mechanisms of action for medications used to treat osteoporosis
Describe lifestyle modifications to help decrease the risk of fractures
The following individuals were involved in developing this activity: Amanda Mayer, PharmD, Anna S. Smith, MPH, BSN-RN, Jeff Goldberg, PharmD, BCPP, and Pamela M. Sardo, PharmD, BS. Pamela Sardo, PharmD, BS, was an employee of Rhythm Pharmaceuticals until March 2022 and has no conflicts of interest or relationships regarding the subject matter discussed. There are no financial relationships relevant to this activity to report or disclose by any of the individuals involved in the development of this activity.
© RxCe.com LLC 2022: All rights reserved. No reproduction of all or part of any content herein is allowed without the prior, written permission of RxCe.com LLC.
Osteoporosis is a common bone disease that affects over 10 million adults in the United States. Osteoporosis may lead to an increased risk of fractures due to weakening bone tissue, structure, and strength. Screening and evaluation are important to help diagnose osteoporosis. There is no cure for osteoporosis; however, several FDA-approved medications can help reduce fracture rates for patients with osteoporosis. Current FDA-approved pharmacologic options include bisphosphonates, estrogen-related therapy, parathyroid hormone analogs, RANK-ligand inhibitor, sclerostin inhibitor, and calcitonin salmon. Along with medications, several lifestyle modifications can help reduce fracture risks in patients with osteoporosis or low bone density.
Overview of Osteoporosis
Osteoporosis is a bone disorder characterized by weakening bone tissue, structure, and strength.1-4 Low bone mass or low bone density are the terms that have replaced the highly used term osteopenia. Many practitioners still use the term osteopenia; however, low bone mass or density is now preferred.5
This common bone disease may lead to an increased risk of fractures.1 Osteoporosis is complicated by fractures that indicate bone fragility and an increased risk of future fracture.2,3 Vertebral compression fractures are the most common type of fracture.2,4 These fractures may be associated with a 5- fold increased risk of additional vertebral fractures and a 2- to 3-fold increased risk for fractures at other sites.3
Osteoporosis is typically associated with women but it is also diagnosed in men.6 Although osteoporosis is less prevalent in men than women, it is estimated that 30% of all hip fractures occur in men. Moreover, some studies have shown that the fracture-related mortality rate is higher in men than in women.7
When left untreated, osteoporosis may lead to recurrent fractures, resulting in disability and premature death. Some patients may not perceive fractures as significant; however, fractures can place a large medical, personal, and financial burden on individuals and their families.3 Fractures may result in depression and loss of self-esteem due to patients trying to manage pain, physical limitations, and loss of independence post-fracture.3 The risk of death increases in the year following a hip fracture. It has been reported that many patients (as high as 80-95% in some settings) discharge after a hip fracture repair without anti-fracture treatment or a management plan.3,8,9
Lewiecki, et al. (2019), reported that osteoporosis resulted in $57 billion dollars in healthcare costs.10 The high cost of treating osteoporosis is partly driven by the low percentage of patients who receive early treatment for the condition, leading to future fractures that increase costs.10 Williams, et al. (2021) studied Medicare patients with osteoporosis-related fractures and confirmed Lewiecki, et al.’s findings that medical care for osteoporosis-related fractures is costly.11 Williams, et al. found that costs of care were disproportionately higher for men and for patients who suffered subsequent fractures.11 Williams, et al., added that osteoporosis-related fractures also impacted healthcare costs generally since this condition affects a patient’s overall health status.11 When a patient’s overall health status is impacted, he or she will require extended hospital stays, and long-term care because of their loss of independence.10 All of this leads to increased healthcare costs.
There is no cure for osteoporosis; however, there are FDA-approved medications that can help reduce fracture rates for individuals with osteoporosis. A key tool to help prevent bone fractures is screening for osteoporosis in older adults to help identify the disease early and develop strategies that help prevent its progression.7
Lewiecki, et al. (2019), report that osteoporosis affects over 10 million adults in the United States.10 Even with that high number, it is likely underdiagnosed and undertreated. In 2018, there were 1.9 million fractures, which is expected to rise with the aging population.10 The utilization of dual- energy x-ray absorptiometry (DEXA) scans is low, at a reported 11.3% in 2014 for women ages 65 years and up. Lewiecki, et al., reported that the low utilization of DEXA scans may be due to a decline in Medicare reimbursement for office-based scans. A Medicare analysis found that only 30% of patients received treatment for osteoporosis over 12 months following.10
Fractures are most commonly seen in the vertebrae (lumbar spine), proximal femur (hip), and distal forearm (wrist). Fractures should indicate the need for further assessment and treatment in patients over the age of 50. Fractures that are not considered osteoporotic fractures include fractures of the fingers, toes, face, and skull, as they are typically related to trauma and not bone fragility. Even in the case of fractures caused by considerable trauma, most fractures that occur in older adults are partly due to low bone mass.3
Hip fractures are very significant, with as many as 60% of patients who suffer a hip fracture being unable to regain full pre-fracture independence.3,12 Patient mortality one year after a hip fracture has been estimated to be from 8.4%-36%. Mortality after a hip fracture is higher in men than women. Vertebral fractures are not associated with as high a mortality rate, but can often cause pain, deformity, disability, and in some cases, premature death. Some vertebral fractures can be clinically apparent, whereas others are clinically silent but may increase the risk for additional fractures. Wrist fractures tend to occur earlier in life (50-60 years of age) and can help to identify individuals with increased bone fragility who need to start treatment sooner.3
Bone Pathophysiology and Osteoporosis
Bone is constantly adapting and undergoing cycles of modeling and remodeling. These cycles help the body to adapt to mechanical demands and maintain skeletal integrity by removing damaged bone and maintaining strength. Osteoclasts are in charge of bone resorption, and osteoblasts are in charge of bone formation. Osteoporosis results from bone resorption that occurs without bone formation. Fractures result from the lack of osteoblastic bone formation, which causes bones to become weak and fragile.13,14
Childhood and adolescence are critical times in the bone life cycle where modeling occurs. During this time, new bone is formed at one site, and old bone is removed from another site of that same area.3 Bone remodeling continues throughout life and is characterized by the activation phase, the resorption phase, the reversal phase, and the formation phase. Osteoclasts are recruited during the activation phase, which leads to the osteoclasts resorbing bone during the resorption phase. Osteoclasts then undergo apoptosis (cell death) during the reversal phase, which leads to the recruitment of osteoblasts. Osteoblasts work in the formation phase by introducing new, organic bone matrix that will mineralize. When peak bone mass occurs, remodeling and bone mass are stable for approximately a decade or two prior to age-related bone loss.15
Osteoporosis Screening Recommendations
Treatment of osteoporosis can be thought of in two stages: primary care and specialist care. During primary care treatment, a patient should be screened for osteoporosis. Screening and evaluation are important to help diagnose osteoporosis.16 Screening densitometry should be performed in all women aged 65 and up and men 70 and up. If an individual has risk factors for osteoporosis, including younger postmenopausal women ages 50-64 and men ages 50-69, screening is also recommended. Men and women who present with fractures should obtain a mean bone mineral density (BMD) test. Specific risk factors for bone loss, including glucocorticoid use or significant
fracture history, are indications for obtaining bone density measurements in healthy young men or premenopausal women.3
Screening includes a patient’s complete medical and familial history as well as a physical examination. The screening should include an assessment of muscle strength as well as assessing clinical risk factors for fractures and the patient’s current risk for falls. Primary care visits should include a discussion about early prevention strategies, including lifestyle modifications. If needed, a patient can be recommended for further diagnostics for osteoporosis. If it is determined that a patient requires specialist care, a specialist will begin by considering a differential diagnosis of the patient’s symptoms. The specialist then evaluates all fracture risk factors.16
Screening tools that are available to assess osteoporosis risk include the Osteoporosis Risk Assessment Instrument (ORAI), Osteoporosis Index of Risk (OSIRIS), Osteoporosis Self-Assessment Tool (OST), Simple Calculated Osteoporosis Risk Estimation (SCORE). The tools listed above are moderately accurate at predicting osteoporosis and consist of a brief questionnaire to help determine if further assessment is needed. The most commonly used test to help diagnose osteoporosis is a DEXA scan which determines bone mineral density.17
A Z-score refers to the number of standard deviations above or below the BMD for persons of the same age, sex, and ethnicity. A T-score refers to the number of standard deviations above or below the mean BMD of a young adult reference population.3 The Z-score and T-score take a patient-specific BMD and compare it to the mean BMD of the reference population.3 Diagnostic T-scores are measured by central DEXA at the lumbar spine and femoral neck.18 Increased BMD has been associated with increased bone strength, which has been predicted to reduce fracture risk.19 As mentioned above, a bone mineral density test is recommended for women aged ≥ 65 years and men aged ≥ 70 years, postmenopausal women and men aged 50–69 years,
based on risk profile, and postmenopausal women and men aged ≥ 50 years with a history of adult-age fracture.3
Postmenopausal Women and Men Aged 50 and Older
The World Health Organization (WHO) has BMD criteria for osteoporosis in postmenopausal women and men aged 50 and older, as listed in Table 1 below.3 These criteria should not be the sole determinant of fracture risk but are sufficient for a diagnosis of osteoporosis.3
Table 1: BMD criteria for Osteoporosis
|BMD within 1.0 standard deviations of the mean for a young-adult reference population
|T-score of -1.0 and above
|Low Bone Mass
|BMD between 1.0 and 2.5 standard deviations below the mean for a young-adult reference population
T-score between -1.0
|BMD of 2.5 or more standard deviations below the mean for a young-adult reference population
|T-score at or below - 2.5
In addition to the T-score, the WHO describes clinical criteria, also which should not be the sole determinant of fracture risk but are sufficient for a diagnosis of osteoporosis.3 These criteria should not be the sole determinant of fracture risk but are sufficient for a diagnosis of osteoporosis.3
Incident fracture includes hip, vertebral, and/or forearm fractures consistent with osteoporosis.
Fracture Risk Assessment Tool (FRAX®) score, which includes a T- score between -1.0 and -2.5 at the femoral neck or total hip by
DEXA along with a FRAX®-projected 10-year risk of ≥ 3% for hip fracture and/or >20% for major osteoporosis-related fracture.3
The FRAX® calculates the 10-year probability of hip fracture and major osteoporotic fracture. The FRAX® takes into account age, BMD at the femoral neck, female sex, parental history of hip fracture, rheumatoid arthritis, alcohol intake, low body mass index, oral glucocorticoid intake of 5 or more mg/day of prednisone for more than 3 months, prior osteoporotic fracture, current smoking status, and secondary causes of osteoporosis. In the United States, calculating FRAX® scores requires selecting either Caucasian, Black, Hispanic, or Asian for each patient, as data indicates that even at the same BMD, fracture risk can be different among these populations.3
Premenopausal Women and Men less than 50 Years of Age
The diagnostic criteria for normal, low bone density, and osteoporosis are different in premenopausal women and men less than 50 years of age. In these populations, densitometric criteria alone should not be used. The International Society for Clinical Densitometry (ISCD) recommends using ethnicity- or race-adjusted Z-scores in individuals between 20 and 50 years old. A Z-score of -2.0 or lower is classified as low BMD in this population. A Z- score above -2.0 is classified as within the expected range.12 Data from the National Health and Nutrition Examination Survey from 2017-2018 found that the age-adjusted prevalence of osteoporosis among adults ages 50 and older was 12.6%.20 This number was higher among women (19.6%) than men (4.4%) and included osteoporosis at either the femur neck, lumbar spine, or both. Prevalence of osteoporosis increased at a higher age, with 17.7% of individuals 65 years and over having osteoporosis compared to 8.4% of individuals in the 50-64 age range.20 Low bone mass was a precursor to osteoporosis and was prevalent in either the femur neck or lumbar spine or both, in 43.1% of adults aged 50 and over, higher numbers in women (51.5%) than men (33.5%).20 Non-Hispanic white and Hispanic-American women have the highest risk for fracture at any site. Non-Hispanic White men have the highest incidence of hip fractures.3
Differential diagnoses that may trigger secondary osteoporosis include hypogonadism, monoclonal gammopathy, osteomalacia, primary hyperparathyroidism, multiple myeloma, and Paget’s disease.21,22 Additional secondary causes of osteoporosis include type 1 diabetes, osteogenesis imperfecta in adults, premature menopause, chronic malnutrition or malabsorption, and chronic liver disease.3 Vertebral deformities such as vertebral wedging may mimic some of the visual signs of osteoporosis, including spinal deformity and height loss. Non-osteoporotic spinal diseases can cause vertebral deformities and have been observed in patients with disorders of intervertebral disc cartilage end plates, such as Scheuermann’s disease. Patients with non-osteoporotic short vertebral height have similar bone mineral densities to patients without osteoporosis. Visual appearance is not a reliable diagnostic tool, and further testing should be done to differentiate vertebral deformities and vertebral fractures when diagnosing osteoporosis. 2
Factors that may contribute to fracture rates include BMD, cortical thickness, skeletal geometry, access to healthcare, and comorbidities. Access to healthcare, including screening, nutrition, lifestyle, and follow-up, are challenges to preventing and treating osteoporosis. An example of healthcare disparities includes the finding that Native Americans with similar BMD to Non- Hispanic Whites had a higher rate of hip fractures which may be correlated to decreased access to healthcare.3
Osteoporosis often progresses without any symptoms until a fracture occurs. A loss of 4 cm or more in height and the development of a stoop or curved upper back are the only two visible signs that may suggest bone loss due to osteoporosis. These two visible signs may indicate possible spine fractures as they are often extremely painful; however, some individuals experience them without much pain.23
Non-modifiable Risk Factors
Non-modifiable risk factors of osteoporosis include age, gender, family history of osteoporosis, previous fracture, menopause or hysterectomy, Caucasian race, poor health, medications, and certain other diseases.16,24 Women who have experienced menopause or a hysterectomy lose bone faster due to a lack of estrogen which has a protective effect on bone. Women who experience menopause before age 45 or have had a hysterectomy are put at an even greater risk.24
Several medications have side effects linked to osteoporosis or increased fracture risk. When an appropriate alternative is available, avoiding these medications in patients with osteoporosis or other nonmodifiable risk factors is best. Using long-term glucocorticoids, such as prednisone, for three or more months, increases the risk of fracture. Certain steroid hormones, including medroxyprogesterone acetate, luteinizing hormone-releasing hormone agonists, and hormone (androgen) deprivation therapy, can also increase risks. Other medications that may affect BMD include proton pump inhibitors, certain diabetes medications, antidepressants, anxiolytics, sedatives and neuroleptics, thyroid hormone treatment, immunosuppressants, aromatase inhibitors, chemotherapy agents, antipsychotics, anticonvulsants, anti-epileptics, and anticoagulants.24
Disease states that may weaken bones and increase the risk of osteoporosis and fractures include rheumatoid arthritis, nutritional or gastrointestinal problems, COPD and asthma, endocrine disorders (that include hypogonadal states), immobility, chronic kidney disease, HIV/AIDS, cancers, hematological disorders, psychophysiological disorders, and mental illness. Rheumatoid arthritis is a major and common risk factor. Lactose intolerance, Crohn's disease, inflammatory bowel disease, and celiac disease are examples of nutritional/gastrointestinal problems that may increase risk. Diabetes, Cushing’s syndrome, hyperparathyroidism, Turner/Klinefelter syndrome, and amenorrhea are examples of endocrine disorders that may affect bone strength.24,25 Prostate and breast cancer may also affect bone
strength. Dementia and anorexia nervosa are examples of psychophysiological disorders or mental illnesses in which bone strength may become compromised.24
Modifiable Risk Factors
Modifiable risk factors for osteoporosis include excessive alcohol intake, smoking, low body mass index, poor nutrition, vitamin D deficiency, eating disorders, not enough exercise, low dietary calcium intake, excessive coffee consumption, a sedentary lifestyle, lack of mobility, and frequent falls.16,24 Several dietary changes can be made in individuals with a high risk of developing osteoporosis. Diets rich in calcium, protein, fruits, and vegetables can help to benefit bone health. Eating disorders can also be attributed to causing low bone density as they can result in estrogen deficiency, and if dietary calcium intake is insufficient, the combination of these factors can cause rapid bone loss. Many individuals may need to supplement their diets with vitamin D as many individuals, particularly in the winter months in northern latitudes, can develop low levels of vitamin D.24
The use of 5 or more drugs or the use of potentially inappropriate medications is considered polypharmacy and has been associated with an increased risk of hip fracture. Patients with a hefty medication load may also be at higher risk for falls due to dizziness caused by many medications. Proton pump inhibitors are also associated with lower trabecular bone density in older individuals. Some hypotheses on how proton pump inhibitors may affect bone density are interference with bisphosphonates, decreased bioavailability of micronutrients and vitamins that are necessary for bone metabolism, decreased calcium bioavailability due to hypergastrinemia, and increase in PTH levels.14
Fall and Fracture Reducing Lifestyle Modifications
Patients should be screened for fall risk yearly or any time a patient presents with an acute fall.26 If a patient answers YES to any of the following three questions, they are considered at risk.
Do you feel unsteady when standing or walking?
Do you worry about falling?
Have you fallen in the past year? If YES the patient should be asked “How many times?” and “Were you injured?”
Patients who are screened and determined to be at risk should be evaluated for gait, strength, and balance. Other assessments that may be performed to help assess a patient's fall risk factors include a Snellen eye test to check visual acuity as well as measuring orthostatic blood pressure.26
Medical risk factors for falls that may cause fractures include advanced age, arthritis, female gender, poor vision, urinary urgency or incontinence, previous fall, orthostatic hypotension, impaired transfer and mobility, certain medications, and malnutrition/parenteral nutrition. Medications that cause dizziness or sedation, such as narcotic analgesics, anticonvulsants, and psychotropics, can be fall risk factors. Psychological risk factors such as anxiety, agitation, depression, decreased cognitive acuity, and fear of falling may also present in patients who have fallen or are at risk of falling.3
Patients may also be at risk for falls due to neurological and musculoskeletal risk factors such as poor balance, weak muscles/sarcopenia, gait disturbances, abnormal spinal curvature, reduced proprioception, Alzheimer’s disease, delirium, Parkinson’s disease, and stroke. Diseases and treatments that may cause sedation, dizziness, weakness, and lack of coordination also present a risk.3
Environmental risk factors that are typically modifiable include clutter or obstacles in the walking path, rugs, low lighting, stairs, slippery outdoor conditions, and a lack of assistive devices around the home.3 Patients should be counseled on these risks and evaluate how modifications in their home environment may be made to help decrease the risk of falls.
Quality of Life Impacts
While fractures may be the most obvious physical consequence of osteoporosis, other long-term effects may occur that change a patient’s quality of life. Chronic pain due to osteoporosis may cause reduced physical performance, including difficulty performing activities of daily living. Some patients may experience loss of height and upper back kyphosis, commonly known as “dowager’s hump.” Gastrointestinal disorders may also occur, such as bloating, pain, difficulty passing stools, and a sense of fullness. These physical consequences may also be accompanied by social and psychological impacts. Sleep disorders, depression, social isolation, decreased quality of life, and disability may occur. A patient may also experience deterioration of economic and financial standing that may occur due to the above-stated consequences.16
Patient Education and General Treatment Considerations
Patients diagnosed with osteoporosis should receive an education tailored to osteoporosis and its treatment options. These education points include physical therapy, fall prevention, vitamin D supplementation, diet modification, pharmaceutical treatment, and monitoring. Using the safest and most effective medications and implementing non-medication-related treatment, such as exercise, to improve muscle strength and balance can help reduce the risk of osteoporosis and the consequences of fractures.16
As with any disease state, adherence is one of the most important considerations in treatment. Patients should follow administration instructions for the best outcomes with the least likelihood of developing side effects. In
specific, bisphosphonate therapy has very structured administration requirements that are discussed below. When choosing therapy for a patient, a positive aspect of the treatment of osteoporosis is there are daily, weekly, monthly, twice-yearly, and yearly options that can help with compliance. Patients diagnosed with osteoporosis may not feel any symptoms; therefore, may have a difficult time starting or adhering to medications. Understanding a patient's attitude and thoughts regarding treatment is helpful when tailoring information and presenting motivational interventions.14 Patients should understand that even with successful treatment that can be defined as an increase in BMD, reduction in fracture risk, and improved T-scores, they will still have osteoporosis and should not get discouraged or discontinue therapy. If the T-score improves and a patient is classified as having low bone density when previously classified as having osteoporosis, caution should be taken when changing a patient’s diagnosis as that may limit treatment options which could decrease bone health.3
Post-fracture osteoporosis care was at one time uncommon, particularly among Black and male patients.27,28 This is the lowest population group to have osteoporosis, since women, especially White women, are the highest risk group.3 Care has increased over time, but for most patients, a fracture was insufficient to trigger effective secondary prevention, especially for patients without pre-fracture osteoporosis attention. Clinicians and policymakers must consider effective remedies to this persistent care gap.27
Nonpharmacologic Treatment for Osteoporosis
Regular exercise can benefit individuals with osteoporosis by helping to reduce pain, prevent falls and fractures, improve mobility, help to activate the sensorimotor system, and subjectively improve quality of life. Kinesitherapy (movement therapy) can be used at all stages of osteoporosis and includes things like education on proper posture as well as doing anti-kyphosis exercises to help treat a rounded upper back. Commonly used exercises include breathing exercises that improve posture, resistance exercises, balance exercises, training for everyday activity, and water exercises.16
Pharmacologic Treatment Options
Management of osteoporosis must be individualized to the patient. Current FDA-approved pharmacologic options include bisphosphonates, estrogen-related therapy, parathyroid hormone analogs, a RANK-ligand inhibitor, a sclerostin inhibitor, and calcitonin salmon.3 Most agents work to inhibit bone resorption with the exception of teriparatide and abaloparatide, which causes bone formation, and romosozumab, which causes bone formation as well as inhibits bone resorption.14 Table 2 summarizes pharmacological options for treating osteoporosis.
Table 2: Summary of Osteoporosis Pharmacologic Treatment Options
- Inhibits bone resorption
|alendronate, ibandronate, risedronate, zoledronic acid
- Inhibits bone resorption
|estrogen, raloxifene, conjugated estrogens/bazedoxifene
Parathyroid hormone analogs
- Causes bone formation
- Inhibits bone resorption
- Causes bone formation and inhibits bone resorption
- Inhibits bone resorption
Preventative Vitamins and Minerals
Vitamin D, in combination with calcium, has been effective in helping protect against hip and non-vertebral fractures.14 The Institute of Medicine’s (IOM) recommendation for calcium intake is 1000 mg/day for men ages 19- 70 and women ages 19-50. Recommended calcium intake increases to 1200 mg/day for women 51 and older and men 71 and older.29 Calcium helps the endocrine feedback system with vitamin D and parathyroid hormone to help inhibit bone resorption.14 Calcium supplementation should be combined with vitamin D as vitamin D facilitates calcium absorption, which is necessary for the mineralization of bone. The IOM recommends adults take 600 IU/day of vitamin D until age 70 and 800 IU/day for adults 71 and older.29 The Bone Health and Osteoporosis Foundation (BHOF) recommends slightly higher doses of vitamin D intake at 800 to 1000 IU of vitamin D for adults ages 50 and up.30 The preferred method of calcium intake is through dietary sources. Calcium and vitamin D supplement options are available over the counter; however, occasionally, prescriptions will be written for these treatments. Vitamin D 50,000 IU and above are available by prescription only.
The main adverse effects to consider with calcium are hypercalcemia, urolithiasis, gastrointestinal symptoms, and vitamin D intoxication with vitamin D supplementation.14 Supplemental calcium in excess of 1200 to 1500 mg/day does not show evidence of additional benefits to bone health and supplementation above that range may increase the risk of developing kidney stones.31 A counseling point for over-the-counter calcium supplements to consider is calcium carbonate is best taken with food as it requires stomach acid for absorption. Calcium citrate can be taken with or without food. If stomach discomfort occurs while taking calcium carbonate, individuals may take it with food or in multiple smaller doses or switch to the citrate formulation.3 Vitamin D3, also known as cholecalciferol, is the form of vitamin D produced in humans and is the preferable source of vitamin D supplementation. Vitamin D2, also known as ergocalciferol, is also effective and may be preferred by individuals who follow a strict vegan/vegetarian diet as it is derived from plant sources.3
Agents Inhibiting Bone Resorption
Agents inhibiting bone resorption, such as bisphosphonates, denosumab, estrogens, and raloxifene, are antiresorptive agents. Teriparatide and romosozumab are considered osteoanabolic therapy as they activate bone formation due to their effects on osteoblasts. These osteoanabolic therapies can be underutilized due to cost concerns and a potential underestimation of benefits.14
In some cases, combination and/or sequential use of osteoanabolic and potent antiresorptive therapies have been shown to help increase BMD. Combination therapy may be appropriate in high-risk settings or if the disease process worsens during monotherapy. When using monotherapy, a common starting point is antiresorptive therapy, then an osteoanabolic option if the response to antiresorptive agents is insufficient.3
Bisphosphonates, such as alendronate, ibandronate, risedronate, and zoledronic acid (also known as zoledronate), are commonly used for the treatment of osteoporosis.16 Bisphosphonates attach to hydroxyapatite binding sites on bone surfaces and prevent osteoclastic activity and cause osteoclast apoptosis to help inhibit bone resorption.14 Calcium and vitamin D supplements, along with regular lab work, are recommended when using bisphosphonate therapy. Serum creatinine/BUN should be performed prior to initial administration and periodically during treatment as renal impairment dose adjustments should be made, and bisphosphonates should not be given in patients with an estimated GFR below 30-35 mL/min.3 Serum calcium levels should be obtained as bisphosphonates may cause or exacerbate hypocalcemia.3 Other labs obtained at baseline and periodically while on bisphosphonate therapy include serum 25(OH)hydroxyvitamin D concentrations, serum alkaline phosphatase, and serum phosphate.
Alendronate and ibandronate are available in tablets that can be taken daily or weekly. Risedronate can be taken orally in a tablet daily, weekly, or monthly. Ibandronate is also available as an injection, given every 3 months, and is only used to reduce the risk of spinal fracture in postmenopausal osteoporosis and is not recommended for men. Zoledronic acid is available as a solution for infusion which is given once yearly. An important counseling point with oral bisphosphonates is that they must be taken on an empty stomach and the patient must remain upright for at least 30 minutes following the dose. For oral options, it is important to note the differing dosages for the weekly and daily administration as the weekly doses are often much higher than the daily doses and can be a source of error in prescribing and dispensing.
Alendronate, risedronate, ibandronate, pamidronate, and zoledronic acid are considered first-line therapy for osteoporosis in postmenopausal women. Alendronate, risedronate, and zoledronic acid can all be used for glucocorticoid-induced osteoporosis. These agents are also used for osteoporosis prevention and are considered to have equal benefits across the class for increasing bone mineral density. Alendronate, risedronate, and zoledronic acid reduce vertebral and non-vertebral fractures. Ibandronate has only been shown to reduce the incidence of vertebral fractures, making the other bisphosphonate options more desirable for use.3
Osteonecrosis (death of bone tissue) of the jaw is a risk of bisphosphonate therapy. Regular dental screenings and good oral hygiene practices can help detect and lower the risk of drug-related osteonecrosis of the jaw. Patients taking oral bisphosphonates should be warned of the risk for esophageal, stomach, or intestinal ulcers, esophagitis, and esophageal erosions. Acute phase reactions such as fever and other flu-like symptoms are reported with IV zoledronic acid use. Bisphosphonate therapy should be periodically reassessed and patients with osteoporosis with low fracture risk may be able to discontinue therapy after 3 to 5 years while still receiving consistent monitoring. The optimal treatment duration for bisphosphonates is still undetermined; however, patients with osteoporosis and low to moderate fracture risk may consider discontinuing therapy after 3 to 5 years and high-
risk postmenopausal women may have a treatment duration of 5 to 10 years. Fracture risk should be periodically reassessed after discontinuation of bisphosphonates. These medications can affect renal function and use is contraindicated in patients with an estimated glomerular filtration rate (GFR) of 30-35 mL/min or below.3
Calcium and other multivalent cations should not be administered at the same time as bisphosphonates. The bisphosphonate should be taken 30 to 60 minutes before oral medications such as antacids, supplements, or vitamins as well as any other dietary foods to avoid the interaction. NSAIDs should be taken with caution in patients on bisphosphonate therapy due to the increased risk of GI irritation. Medications with a high risk of nephrotoxicity, such as cyclosporine and aminoglycosides, can also increase the risk of nephrotoxicity when used in combination with pamidronate or zoledronic acid infusions and frequent monitoring for renal toxicity should be done if concomitant administration is required. Dental examinations and preventative dentistry should be obtained before bisphosphonate therapy and every 6 months thereafter. Patients on bisphosphonate therapy should avoid oral surgery if possible. Current literature does not show a significant benefit to bisphosphonate holidays surrounding oral procedures; however, the current standard of practice includes bisphosphonate holidays of two months before and up to three months after an invasive dental procedure if the patient has been taking bisphosphonates for more than four years to help decrease the likelihood of osteonecrosis.32 Developing osteonecrosis of the jaw may be more prevalent in patients who receive dental extractions along with poor oral hygiene, cancer diagnosis, concomitant therapies, and comorbidities. Patients who do not remain upright for at least 30 minutes following a dose of oral bisphosphonates are at increased risk of developing upper gastrointestinal mucosal irritation. Patients with hypocalcemia should receive corrective treatment prior to initiation of bisphosphonate therapy as it may worsen the issue or even cause it in patients without prior hypocalcemia issues.
Oral bisphosphonates must be taken on an empty stomach and the patient must remain upright for at least 30 minutes following the dose.
Bisphosphonate Therapy Clinical Pearl
Bisphosphonate holidays may be considered after 3 years of intravenous therapy or 5 years of oral therapy in patients who appear to have a modest risk for fracture. These patients qualify with a T-score greater than -2.5 and no recent fractures. A bisphosphonate holiday is the temporary suspension of the medication for up to 5 years with the expectation of prolonged skeletal retention from previous treatment. An advantage to the bisphosphonate holiday is the potential reduction in risk for osteonecrosis of the jaw and atypical femoral fracture. Patients at high fracture risk should continue therapy with an oral bisphosphonate for up to 10 years and intravenous zoledronic acid for up to 6 years. Patients on bisphosphonate holidays may be evaluated every 1 to 2 years to assess the need for resuming treatment.3
The FDA has approved estrogen/hormone therapy (ET/HT) for the prevention of osteoporosis associated with menopause. Estrogen alone is used in women who have had a hysterectomy, and combined estrogen and progestin therapy, known as hormone therapy (HT), is required in women with an intact uterus to help protect the uterine lining.3 Hormone therapy has been shown to reduce fractures in the spine, hip, and non-vertebral skeleton by 35%, 28%, and 22%, respectively.33 An advantage to ET/HT is the wide variety of preparations, including oral and transdermal, which are available in estrogen only, progesterone only, and combination products. Dosing and formulation should be individualized to the patient's needs. Upon discontinuation of ET/HT, bone loss can occur rapidly. Estrogen/hormone therapy should not be considered solely for fracture prevention if other approved non-estrogen treatments have not been carefully considered first.3
A combination product of conjugated estrogens and bazedoxifene, known under the brand name Duavee, can be considered in postmenopausal women at significant risk for osteoporosis who have not had a hysterectomy. The dose is one tablet (conjugated estrogens 0.45 mg, bazedoxifene 20 mg) orally once daily. This product is a combination of natural estrogens that are derived from the urine of pregnant mares with bazedoxifene, which is a third- generation selective estrogen receptor modifier (SERM). Bazedoxifene adds an estrogen agonist/antagonist component which decreases the risk of endometrial hyperplasia. Like ET/HT, it should not be used before carefully considering non-estrogen regimens. The estrogens generally do not reverse already developed bone density loss, but they do help to prevent osteoporosis associated with menopause onset. Bazedoxifene helps to reduce endometrial overgrowth in postmenopausal women taking estrogen and eliminates the need for progestins in females who have not undergone hysterectomy.3 This product was shown to decrease the risk of new vertebral fractures for women with postmenopausal osteoporosis; however, the combination did not demonstrate a decreased risk of nonvertebral fractures.34
Raloxifene, under the brand name Evista, is a SERM that may be used to treat osteoporosis by enhancing osteoclast apoptosis.14,16 Raloxifene is FDA-approved for the treatment of osteoporosis and for osteoporosis prophylaxis in postmenopausal women.3 A decrease in circulating estrogen in postmenopausal women can lead to enhanced bone resorption. Raloxifene has estrogen-like effects, appearing to act as an estrogen agonist on bone, reducing bone resorption and increasing bone mineral density. Raloxifene is administered at a dose of 60 mg by mouth once daily, without regard to meals.3 Raloxifene has been shown to reduce vertebral fractures, but it is not typically used as a first-line therapy as it does not help to reduce hip or nonvertebral fractures. The incidence reduction of vertebral fractures in patients taking raloxifene is about 30-40% if a patient had a previous vertebral fracture and about 55% in a patient without a previous vertebral fracture.3 Raloxifene may be considered in postmenopausal patients with an elevated risk of breast cancer for the prevention of bone loss. Raloxifene is also used for breast cancer prophylaxis in postmenopausal women with osteoporosis or
Raloxifene is contraindicated in individuals with acute thromboembolism or a history of thromboembolic disease.
Estrogen-Related Therapy Clinical Pearl
in postmenopausal women at high risk for developing breast cancer. If a patient is taking raloxifene for breast cancer prophylaxis but is also at high risk of hip fracture, they may combine therapy with a bisphosphonate or denosumab for added hip fracture reduction. The risks and benefits of combined treatment with raloxifene and bisphosphonates or denosumab are unknown and patients should be monitored for adverse effects.34 Raloxifene may cause hot flashes within the first 6 months of treatment in up to 28% of patients. Raloxifene is contraindicated in individuals with acute thromboembolism or a history of thromboembolic disease as it has been associated with an increased risk of venous thromboembolism, with the greatest risk occurring in the first 4 months of treatment. Raloxifene is only for use in postmenopausal women, and safety has not been established and is not recommended in premenopausal women.35
Parathyroid Hormone Analogs
Teriparatide is a parathyroid hormone (PTH) type bone stimulating agent that has been used in severe osteoporosis with fractures once other drugs have been proven to be ineffective.16 Parathyroid hormone plays a key role in the regulation of calcium homeostasis and increases bone formation and mass.14 Teriparatide can be used in men and women and is indicated for the treatment of osteoporosis in patients with a high risk of fracture or patients who have failed or are intolerant to other available therapies.36 High-risk fracture patients may consider teriparatide therapy. High-risk fracture patients include postmenopausal women, men with primary or hypogonadal osteoporosis, and glucocorticoid-induced osteoporosis. Teriparatide is administered as a once-daily subcutaneous injection of 20 mcg. Teriparatide therapy increased lumbar spine bone density by 9.5% and hip bone density
by 2.6% with 18 to 19 months of therapy and reduced the risk of vertebral fracture by 56% in high-risk women in clinical trials.37 Teriparatide is available in two formulations, Forteo and Bonsity.36,38 Bonsity should not be used for more than 2 years during a patient's lifetime,38 and the use of Forteo for more than 2 years should only be considered if a patient remains at or returns to having a high risk for fracture.36 Both formulations should be followed by treatment with a bisphosphonate or denosumab upon discontinuation to prevent a decrease in bone density and loss of efficacy.34,37,39 Teriparatide was previously limited to 2 years of therapy due to elevated osteosarcoma (a malignant bone tumor) seen in rodent studies; however, in the 15 years of post-marketing studies, increased osteosarcoma has not been observed in humans and the revised teriparatide label states that use for more than 2 years during a patient’s lifetime can be considered. If a patient has other risk factors for osteosarcoma, the use of teriparatide should be avoided.3 Patients with increased risk of osteosarcoma include patients with open epiphyses, metabolic bone disease (including Paget’s disease), bone metastases or history of skeletal malignancies, prior external beam or implant radiation therapy involving the skeleton, and hereditary disorders predisposing to osteosarcoma.36
When administering teriparatide, the first dose should be given in a setting where the patient can sit or lie down and should be monitored for symptoms of orthostatic hypotension. Common adverse reactions include arthralgia and nausea, along with injection site reactions and hypercalcemia.36 Forteo and Bonsity are prefilled syringes that should be stored under refrigeration and injected subcutaneously into the thigh or abdomen. Doses should be given immediately after removal from the refrigerator, and each pen can be used for up to 28 days following the first injection and then should be discarded after that time period.36,38
Abaloparatide, known under the brand name Tymlos, is a synthetic analog of human PTH-related peptide. It can treat osteoporosis in postmenopausal women at high risk for fracture or if they have failure/intolerance to other available therapies. Abaloparatide is administered
Upon discontinuation of these agents, bone loss is rapid and antiresorptive agents, such as bisphosphonates or denosumab, should be considered to prevent a decrease in bone density and loss of efficacy.
Parathyroid Hormone Analogs Therapy Clinical Pearl
as a daily subcutaneous injection in the periumbilical area of the abdomen. Like teriparatide, upon discontinuation, bone loss is rapid and an antiresorptive agent should be considered at this time. Treatment duration should not exceed 24 months due to the potential increased risk of osteosarcoma. Common side effects include leg cramps, nausea, and dizziness. Use of abaloparatide should be avoided in patients with active or recent kidney stones as it may increase urinary calcium.3
Denosumab, commonly known as Prolia, can be used as first-line therapy as well as for the subsequent stages of osteoporosis. Denosumab is a monoclonal antibody that works by inhibiting osteoclast activity which produces an antiresorptive effect that is rapid and reversible if the medication is discontinued.16 Denosumab targets the receptor activator of nuclear factor kappa beta ligand (RANKL), which regulates osteoclast generation, to reduce osteoclast activity and bone resorption.14 Directly inhibiting osteoclast formation and causing apoptosis of mature osteoclasts makes denosumab one of the most potent antiresorptive drugs available.3 Dosing for denosumab can be advantageous as it is 60 mg given subcutaneously twice a year, which can help with compliance. Denosumab has been approved for men and postmenopausal women at risk for fractures and glucocorticoid-induced osteoporosis.14 Two main side effects to be aware of are skin infections at the injection site and hypocalcemia. As with bisphosphonates, denosumab may cause the rare side effect of jaw necrosis.14 Denosumab is contraindicated in patients with pre-existing hypocalcemia. Patients with advanced renal disease are at an increased risk of hypocalcemia. Patients taking denosumab should
Given subcutaneously twice a year, which can help with compliance.
RANK-ligand Therapy Clinical Pearl
be assessed for serum calcium, phosphorous, and magnesium levels before therapy begins, and monitored frequently during therapy.40,41 Adequate calcium and vitamin D intake should be ensured, and a minimum of calcium 1000 mg and vitamin D 400 IU supplementation daily to help reduce the risk of treatment-related hypocalcemia in patients taking denosumab is advised. Caution should be taken as denosumab is also available under the name Xgeva, which is a different dose, approved for other indications. If denosumab is discontinued, alternate antiresorptive therapy should be considered. Alendronate has been shown to preserve bone mass following denosumab discontinuation,3 while teriparatide use upon discontinuation of denosumab has been associated with bone loss at some skeletal sites.31,42
Romosozumab, brand name Evenity, is a parenteral human monoclonal antibody that inhibits sclerostin to stimulate bone formation and inhibit bone resorption.43 Sclerostin is a glycoprotein secreted by osteocytes that acts as a negative regulator of bone formation. Romosozumab is available as a monthly injection of 210 mg subcutaneously and is indicated for osteoporosis in postmenopausal women at high risk for fracture. Postmenopausal women who have failed or been intolerant to other options and individuals who are unable to use oral therapy are also candidates for romosozumab.14 Treatment with romosozumab is limited to 12 doses as the anabolic effect decreases after 12 months of treatment. After discontinuing romosozumab, an anti-resorptive agent, such as a bisphosphonate or denosumab, can be considered if osteoporosis treatment is still indicated.34,37,43
Romosozumab has a boxed warning of increased risks for myocardial infarction, stroke, and cardiovascular death. Romosozumab should not be taken in women who have had a stroke or cardiovascular event in the last year.
Sclerostin Inhibitor Therapy Clinical Pearl
Each full dose consists of two injections that should be given by a healthcare provider. Two separate injection sites should be prepared and recommended sites include the thigh, abdomen, or outer area of the upper arm. Injection sites should be rotated with each dose. The two most common side effects reported with romosozumab are antibody formation, arthralgia, and headache. Romosozumab therapy is contraindicated in patients with preexisting hypocalcemia and patients should be monitored for hypocalcemia development. Romosozumab has a boxed warning of increased risks for myocardial infarction, stroke, and cardiovascular death and should not be taken in women who have had a stroke or cardiovascular event in the last year.3
Calcitonin helps to inhibit bone resorption and decreases serum calcium by binding directly to receptors on the osteoclast surface. Calcitonin in the body is produced in the parafollicular cells of the thyroid gland and is considered a polypeptide hormone. Calcitonin salmon is made synthetically or by using recombinant DNA methods. Calcitonin salmon has a longer duration than human calcitonin and is 40 to 50 times more potent than the human version. Calcitonin salmon is used in women who are more than 5 years post menopause with osteoporosis. Calcitonin salmon is administered daily and may be used intramuscularly, subcutaneously, or intranasally to help prevent bone loss and increase bone density in the vertebral spine. Current guidelines generally recommend against calcitonin salmon in osteoporosis treatment as
its efficacy in preventing vertebral and non-vertebral fractures is not established and options such as bisphosphonates have higher reported bone mineral density increases. Calcitonin salmon is considered a second-line option for women who do not tolerate or refuse other options.3 Pain associated with vertebral crush fractures in many patients may be significantly reduced in patients taking calcitonin, which may help to make early mobilization possible.3
Treatment and Monitoring Considerations
Although many pharmacologic treatment options are available, it is approximated that 30-50% of patients do not take their medications correctly. Some patients who are prescribed treatment never start treatment or follow up taking the medication. Others decide to stop taking the medication shortly after starting. In a publication by Tanski, et al. (2021), the authors discuss published analyses that only one in four patients will follow treatment recommendations.16 The authors list some of the main reasons for treatment non-compliance, including lack of motivation to continue treatment, a patient not having detectable symptoms after initial diagnosis, frustration due to disease progression even while on medication, not believing the medication is helping, and not understanding the consequences of poor compliance. Adherence can be greatly affected by a difficult medication regimen and frequency of dosing. Treatment with agents that may be taken weekly instead of daily can help to improve treatment outcomes.16
Measurable benchmarks such as BMD, fracture incidence, and biochemical markers of bone turnover are helpful for monitoring and reassessment for the therapy and management of osteoporosis. Monitoring may occur yearly to assess treatment response and the need for continued medication or changes. Accurate baseline values help to compare the progression of osteoporosis and treatment efficacy. Goals should be individualized for each patient. Stable BMD and no new fractures are good goals for almost all patients. In some cases, the goal may be T-score
improvement, but this does not necessarily mean they have decreased their risk for fracture if they have not decreased their fall risk.3
The Patient, Osteoporosis, and the Interdisciplinary Team
Care of a patient with osteoporosis may include the primary provider (physician/nurse practitioner/physician's assistant), nurses, a physical therapist, a pharmacist, and a bone specialist. The primary provider or a bone specialist should provide a differential diagnosis to rule out medical conditions that may present with symptoms that are similar to osteoporosis so that the team may develop an effective treatment plan.
Nurses help support individuals diagnosed with osteoporosis or those at risk for osteoporotic fractures. Nurses can enhance the multidisciplinary management of osteoporosis through appropriate assessment and referrals to multidisciplinary members and ease the burden that osteoporosis places on a patient. Nurses can improve the awareness of osteoporosis and advocate for screening in suitable patients.44 Nurses can help identify modifiable risk factors while conducting screening and basic assessments on patients. Nurses may play a crucial role in medication compliance and appointment follow-up, especially in the case of injectable medications that are given at longer intervals.
Pharmacists can help patients by reinforcing education on medications and their benefits. Pharmacists and nurses may also assist the primary physician by motivating a patient to take medications. Tanski, et al. (2021) reported that physicians often fall short when it comes to motivating a patient to adhere to a treatment plan: Physicians “mostly discuss the consequences of non-compliance but are unable to improve patients’ motivation.”16 Tanski, et al., reports that according to patients a good motivator to taking medications was understanding that it helps keep independence and autonomy.16 The pharmacist may reinforce the premise that patients can maintain independence and autonomy if they take their medications as prescribed.16
Pharmacists can also help counsel patients on dietary calcium and vitamin D sources to help maintain healthy bone structure. Pharmacists can help patients with a recommendation for over-the-counter calcium and vitamin D supplementation. Pharmacy technicians play a key role in maintaining over-the-counter supplement inventory, processing prescriptions, and identifying patients who may require additional counseling on medications.
The weakening of bone tissue, structure, and strength characterizes osteoporosis. This common bone disease may lead to an increased risk of fractures. When left untreated, osteoporosis may lead to recurrent fractures, resulting in disability and premature death. Unfortunately, there is no cure for osteoporosis. Some FDA-approved medications can help reduce fracture rates for individuals with osteoporosis. Osteoporosis has modifiable and nonmodifiable risk factors that should be evaluated and screened for these risk factors.
Management of osteoporosis must be individualized to the patient. Current FDA-approved pharmacologic options include bisphosphonates, estrogen-related therapy, parathyroid hormone analogs, a RANK-ligand inhibitor, a sclerostin inhibitor, and calcitonin salmon. Most agents work to inhibit bone resorption, except for teriparatide and abaloparatide, which causes bone formation, and romosozumab, which causes bone formation as well as inhibits bone resorption. Agents inhibiting bone resorption, such as bisphosphonates, denosumab, estrogens, and raloxifene, are considered antiresorptive agents. Teriparatide, abaloparatide, and romosozumab are considered osteoanabolic therapy as they activate bone formation due to their effects on osteoblasts. Measurable benchmarks such as BMD, fracture incidence, and biochemical markers of bone turnover are helpful for monitoring and reassessment for the therapy and management of osteoporosis.
A person may be classified as having osteoporosis with a T-score
of 1 to 2.5.
of -1.0 and above.
between -1.0 and -2.5.
Calculating a FRAX® score takes into account
Age, gender, alcohol intake, and smoking status
Bone mineral density at femoral neck, parental history of hip fracture, rheumatoid arthritis, and low body mass index
Oral glucocorticoid intake, prior osteoporotic fracture, and secondary causes of osteoporosis
All of the above
Negative social and psychological impacts of fractures from osteoporosis may include
bloating and pain.
depression and social isolation.
True or False: Osteoporosis results from bone resorption that occurs without bone formation.
Which medication classes have been associated with lower trabecular bone density in older adults?
Proton pump inhibitors
HMG-CoA reductase inhibitors
An example of a modifiable environmental risk factor for reducing falls can be
to keep lighting in the home to a minimum.
to make sure all walking paths are free of clutter and obstacles.
to use rugs in as many spaces as possible.
to remove railings around the home.
Which of the following agents causes bone formation AND inhibits bone resorption?
The Institute of Medicine recommends calcium intake of mg/day for men ages 19-70 and women ages 19-50.
Which bisphosphonate is available as a yearly infusion?
Raloxifene use is only indicated in
men over 75 years of age.
men ages 18-74.
Kanis JA, Melton LJ 3rd, Christiansen C, Johnston CC, Khaltaev N. The diagnosis of osteoporosis. J Bone Miner Res. 1994;9(8):1137-1141. doi:10.1002/jbmr.5650090802
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Williams SA, Daigle SG, Weiss R, Wang Y, Arora T, Curtis JR. Economic Burden of Osteoporosis-Related Fractures in the US Medicare Population. Ann Pharmacother. 2021;55(7):821-829. doi:10.1177/1060028020970518
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Bouxsein ML, Eastell R, Liu LY, et al. Reply to: Change in Bone Density and Reduction in Fracture Risk: A Meta-Regression of Published Trials. J Bone Miner Res. 2019;34(10):1977-1978. doi:10.1002/jbmr.3837
Sarafrazi N, Wambogo EA, Shepherd JA. Osteoporosis or Low Bone Mass in Older Adults: United States, 2017-2018. NCHS Data Brief. 2021;(405):1-8
Mirza F, Canalis E. Management of endocrine disease: Secondary osteoporosis: pathophysiology and management. Eur J Endocrinol. 2015;173(3):R131-R151. doi:10.1530/EJE-15-0118
Panuccio VA, Tripepi R. Paget's Disease and Secondary Hyperparathyroidism: Is Healing Possible?. Front Cell Dev Biol. 2020;8:399. Published 2020 May 29. doi:10.3389/fcell.2020.00399
Kondo KL. Osteoporotic vertebral compression fractures and vertebral augmentation. Semin Intervent Radiol. 2008;25(4):413-424. doi:10.1055/s-0028-1103000
International Osteoporosis Foundation. Risk Factors. Undated. https://www.osteoporosis.foundation/patients/about-osteoporosis/risk- factors . Accessed April 26, 2023.
Sözen T, Özışık L, Başaran NÇ. An overview and management of osteoporosis. Eur J Rheumatol. 2017;4(1):46-56. doi:10.5152/eurjrheum.2016.048
Centers for Disease Control and Prevention. Algorithm for Fall Risk Screening, Assessment, and Intervention CDC. 2019.
https://www.cdc.gov/steadi/pdf/STEADI-Algorithm-508.pdf. Accessed May 15, 2023.
Liu SK, Munson JC, Bell JE, et al. Quality of osteoporosis care of older Medicare recipients with fragility fractures: 2006 to 2010. J Am Geriatr Soc. 2013;61(11):1855-1862. doi:10.1111/jgs.12507
Watts NB, Adler RA, Bilezikian JP, et al. Osteoporosis in men: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab. 2012;97(6):1802-1822. doi:10.1210/jc.2011-3045.
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Ross AC, Manson JE, Abrams SA, et al. The 2011 Dietary Reference Intakes for Calcium and Vitamin D: what dietetics practitioners need to know. J Am Diet Assoc. 2011;111(4):524-527. doi:10.1016/j.jada.2011.01.004
Jackson RD, LaCroix AZ, Gass M, et al. Calcium plus vitamin D supplementation and the risk of fractures [published correction appears in N Engl J Med. 2006 Mar 9;354(10):1102]. N Engl J Med. 2006;354(7):669-683. doi:10.1056/NEJMoa055218
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Barrionuevo P, Kapoor E, Asi N, et al. Efficacy of Pharmacological Therapies for the Prevention of Fractures in Postmenopausal Women: A Network Meta-Analysis [published correction appears in J Clin Endocrinol Metab. 2021 Mar 8;106(3):e1494]. J Clin Endocrinol Metab. 2019;104(5):1623-1630. doi:10.1210/jc.2019-00192
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Management of Osteoporosis in Postmenopausal Women: The 2021 Position Statement of The North American Menopause Society’’ Editorial
Panel. Management of osteoporosis in postmenopausal women: the 2021 position statement of The North American Menopause Society. Menopause. 2021;28(9):973-997. doi:10.1097/GME.0000000000001831
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Eastell R, Rosen CJ, Black DM, Cheung AM, Murad MH, Shoback D. Pharmacological Management of Osteoporosis in Postmenopausal Women: An Endocrine Society* Clinical Practice Guideline. J Clin Endocrinol Metab. 2019;104(5):1595-1622. doi:10.1210/jc.2019-00221
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The information provided in this course is general in nature, and it is solely designed to provide participants with continuing education credit(s). This course and materials are not meant to substitute for the independent, professional judgment of any participant regarding that participant’s professional practice, including but not limited to patient assessment, diagnosis, treatment, and/or health management. Medical and pharmacy practices, rules, and laws vary from state to state, and this course does not cover the laws of each state; therefore, participants must consult the laws of their state as they relate to their professional practice.
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