Journal of Gerontological Nursing

Clinical Concepts 

Recognition and Treatment of Postmenopausal Osteoporosis

Freda Hannafon, RN, MSN, FNP-C; Mary P. Cadogan, DrPH, RN, GNP-BC, FAAN, FGSA

Abstract

Osteoporosis is a common but often silent condition among older adults. The characteristic pathological changes associated with osteoporosis may go unnoticed until a fracture occurs or a bone density test is performed. Although osteoporosis occurs in men and among premenopausal women, it is most prevalent among postmenopausal women who are the focus of this article. Within the subpopulation of postmenopausal women, there are major differences in risk status, disease severity, and response to treatment. Two individual examples are presented to highlight these differences and to illustrate appropriate assessment and treatment strategies in each scenario. In addition, general nonpharmacological recommendations for postmenopausal women across risk status and disease severity are presented. [Journal of Gerontological Nursing, 40(3), 10–14.]

Ms. Hannafon is Nurse Practitioner, Musculoskeletal Oncology and Osteoporosis, Department of Orthopaedics, University of California Los Angeles (UCLA), Santa Monica; and Dr. Cadogan is Professor, Adjunct Series, UCLA, School of Nursing, Los Angeles, California.

Ms. Hannafon is a speaker and consultant for Lilly USA. Dr. Cadogan has no potential conflicts of interest, financial or otherwise.

Address correspondence to Freda Hannafon, RN, MSN, FNP-C, Nurse Practitioner, UCLA, Musculoskeletal Oncology and Osteoporosis, Department of Orthopaedics, 1250 16th Street, Suite 3142, Santa Monica, CA 90404; e-mail: Fhannafon@mednet.ucla.edu.

Posted Online: February 27, 2014

Abstract

Osteoporosis is a common but often silent condition among older adults. The characteristic pathological changes associated with osteoporosis may go unnoticed until a fracture occurs or a bone density test is performed. Although osteoporosis occurs in men and among premenopausal women, it is most prevalent among postmenopausal women who are the focus of this article. Within the subpopulation of postmenopausal women, there are major differences in risk status, disease severity, and response to treatment. Two individual examples are presented to highlight these differences and to illustrate appropriate assessment and treatment strategies in each scenario. In addition, general nonpharmacological recommendations for postmenopausal women across risk status and disease severity are presented. [Journal of Gerontological Nursing, 40(3), 10–14.]

Ms. Hannafon is Nurse Practitioner, Musculoskeletal Oncology and Osteoporosis, Department of Orthopaedics, University of California Los Angeles (UCLA), Santa Monica; and Dr. Cadogan is Professor, Adjunct Series, UCLA, School of Nursing, Los Angeles, California.

Ms. Hannafon is a speaker and consultant for Lilly USA. Dr. Cadogan has no potential conflicts of interest, financial or otherwise.

Address correspondence to Freda Hannafon, RN, MSN, FNP-C, Nurse Practitioner, UCLA, Musculoskeletal Oncology and Osteoporosis, Department of Orthopaedics, 1250 16th Street, Suite 3142, Santa Monica, CA 90404; e-mail: Fhannafon@mednet.ucla.edu.

Posted Online: February 27, 2014

The National Osteoporosis Foundation (NOF, 2013) describes osteoporosis as a chronic, progressive disease characterized by low bone mass, loss of bone architecture, decreased bone strength, and an increase in the risk of fracture. Currently, 8 million women in the United States are diagnosed with osteoporosis. Another 34 million have low bone mass. More than 2 million osteoporotic fractures occur annually in the United States, and this is expected to reach 3 million by 2020 (U.S. Department of Health and Human Services, 2004). Seventy-one percent of these fractures occur among women, and of those, 89% are experienced by Caucasian women (Cauley, 2013). The lifetime fracture risk for a 50-year-old woman is 40%, but once a fracture occurs, risk of a subsequent fracture increases to 86% (NOF, 2013). Treatment of osteoporosis can decrease fracture risk substantially, but often the disease is unrecognized until a fracture occurs.

Bone and Mineral Metabolism

Bone is a living organism in a constant state of turnover. Bone remodeling is a continual process of resorption and formation of new bone. Remodeling is regulated by hormones such as estrogen and testosterone, as well as parathyroid hormone (PTH), which has direct effects on calcium, vitamin D, and phosphorus. Awareness of the impact of a specific cytokine, RANK ligand (RANKL), has contributed to deeper understanding of the process of increased bone resorption that occurs at menopause (Pacifici, 1996). In a healthy adult woman prior to menopause, the amount of bone that is resorbed is all replaced. When menopause occurs, reduced estrogen levels disrupt the process, leading to increased activity of osteoclasts that resorb bone and decreased activity of osteoblasts that build bone (Riggs, Khosla, & Melton, 1998). In osteoporosis, there is a net loss of bone as well as a change in the quality or microarchitecture of the bone replaced that increases risk for fractures (Seeman, 2013).

Clinical Diagnosis of Osteoporosis

Bone mineral density (BMD), as measured by central dual-energy x-ray absorptiometry (DXA), has long been considered the gold standard for diagnosing osteoporosis. DXA measurement of the hip and spine is used as a predictor of fracture risk and is also used to monitor patients’ progress. The bone density machine reports three values: BMD, T-score, and Z-score. The BMD is reported in grams of mineral per cm2 and then converted into T-scores, which compare to a healthy young adult, and Z-scores, which compare to individuals in the same age group. The T-score is presented as the standard deviation above or below the mean BMD of the reference population (Raisz, 2005). The World Health Organization (WHO) developed a classification system (Table 1) to help interpret BMD results using individual T-scores compared to a reference population of 30-year-old women because peak bone mass is typically achieved at that age (Kanis, Melton, Christiansen, Johnston, & Khaltaev, 1994). In addition to the T-score value, the presence of one or more fragility fractures places an individual in the severe or established osteoporosis category. Clinically, a fragility fracture may be defined as “fractures that can occur following minimal trauma” (NOF, 2013, p. 7).

Definition of Osteoporosis Based on Bone Mineral Density T-Scores and Fragility Fractures

Table 1:

Definition of Osteoporosis Based on Bone Mineral Density T-Scores and Fragility Fractures

In addition to use of the BMD alone for risk prediction, a more comprehensive fracture risk assessment tool (FRAX®) was developed by the WHO to incorporate additional risk factors for prediction of 10-year risk of osteoporotic fractures (available at http://www.shef.ac.uk/FRAX and http://www.nof.org). The following individual risk factors are incorporated into the FRAX tool: age, sex, weight, height, low femoral neck BMD, prior fragility fracture, parental history of hip fracture, current smoking status, long-term use of glucocorticoid agents, rheumatoid arthritis, other causes of secondary osteoporosis, and alcohol intake of two or more defined units daily. The FRAX tool calculates an individual’s 10-year risk of sustaining a major osteoporotic fracture or a femoral neck fracture. If the risk estimate is more than 20% for a major osteoporotic fracture or more than 3% for a hip fracture, treatment is recommended (NOF, 2013). The FRAX tool is best utilized for an individual who has never been treated for osteoporosis, is older than 40, and has a low BMD in the femoral neck as opposed to the spine.

Recognizing risk and preventing fractures is the ultimate goal of osteoporosis diagnosis and treatment. Two individual examples of osteoporosis in postmenopausal women will now be used to illustrate both common and specific treatment strategies based on each woman’s individual risk profile.

Individual Example 1

P.C. is a 58-year-old Caucasian woman who visits the osteoporosis center to discuss her most recent bone density scan. She states that this is her third scan. She has had one every 2 years and was told that the first two scans were “normal.” Her gynecologist called about this most recent scan because it shows a bone loss of 8% in the femoral neck from the scan taken 2 years earlier. The bone density report demonstrated the following scores of the femoral neck: BMD 0.615 g/cm2 and T-score −2.7. Relevant medical history includes menarche at age 14, and menopause at age 54. P.C. denies any history of amenorrhea or other estrogen deficiency, and she has never taken hormone replacement therapy. She has a history of symptoms consistent with irritable bowel syndrome (IBS), but tested negative for celiac disease. At age 24, she fractured her right humerus due to a downhill skiing injury. Her current medications are calcium 600 mg plus 400 international units (IU) of vitamin D once daily. Her diet includes one to two servings of calcium-rich foods daily such as cottage cheese, yogurt, milk, and dark green vegetables. P.C. expresses concern about the recent change in her bone density. She reports being physically active throughout her life. She was a competitive swimmer through high school and college. She still swims 3 to 4 times per week for exercise. She states, “I have always exercised and eaten a healthy diet. I don’t understand why I have this.”

P.C. reports that her mother experienced a wrist fracture from a ground-level fall at age 56, and fell in the nursing home and broke her hip prior to her recent death at age 82. She does not believe that her mother was ever treated for osteoporosis. An older sister does not have osteoporosis. She states that her sister has a large skeletal frame like her father; P.C. has always been small like her mother.

On physical examination, P.C. is 5 feet tall and weighs 110 pounds. She walks with a steady gait and has excellent balance. Spine examination demonstrates good flexion and extension and no focal or generalized kyphosis. She has no pain on palpation or percussion of vertebrae. She can forward flex and touch her fingertips to her toes. Motor strength is 5/5 throughout all extremities. Laboratory results demonstrated a serum calcium of 9.8 mg/dL (normal = 8.4 to 10.2 mg/dL), vitamin D 25 hydroxy of 43 nmol/L (normal = 35 to 105 nmol/L), PTH of 32 pg/mL (normal = 10 to 65 pg/mL), and urine N-telopeptide of 54 (normal for postmenopausal women = 17 to 188 nM BCE/mM creatinine) (American Society for Bone and Mineral Research, 2006). Renal function, thyroid function, and complete blood count were all within normal limits. According to the FRAX tool, her 10-year risk of a major osteoporotic fracture was 20% and a hip fracture was 3%.

According to clinical practice guidelines (NOF, 2013; North American Menopause Society, 2010; Ross et al., 2011; Watts et al., 2010), P.C. was encouraged to meet the daily recommended intake for her age group age of 1,200 mg of calcium and 600 IU of vitamin D through diet and supplements. Although she was encouraged to continue swimming for overall cardiovascular benefit, a recommendation was made that she begin weight-bearing exercise (e.g., simple walking, dancing, running, tennis) for 30 minutes per day. Weight-bearing exercise can modestly increase bone density, but the major effect is on the improvement of the individual’s agility, balance, and overall strength (NOF, 2013). Muscle strengthening activities can also be included for the areas that are most prone to fracture. Other universal guideline recommendations were to avoid smoking and excess alcohol intake.

The following significant findings were discussed with P.C. to develop a mutually agreed upon treatment plan. P.C.’s T-score of −2.7 places her in the osteoporosis category according to WHO criteria, and represented an 8% BMD loss in her hip from the previous scan. The urine N-telopeptide level of 54 indicates ongoing bone loss (Garnero et al., 1996). Finally, her FRAX risk estimate is within the range where pharmacological treatment is recommended (NOF, 2013). P.C.’s fracture risk is increased due to her weight of less than 127 pounds as well as having a first-degree relative (her mother) who had a hip fracture (Cummings et al., 1995). Because of her increased fracture risk, pharmacological therapy was recommended. Current medications for treatment of osteoporosis are shown in Table 2.

Medications for Osteoporosis Treatment

Table 2:

Medications for Osteoporosis Treatment

Bisphosphonates are generally considered first-line treatment for osteoporosis (McClung et al., 2013). Bisphosphonates act by directly entering osteoclasts to inhibit bone resorption (Pinkerton, Thomas, & Dalkin, 2013). P.C. was placed on oral alendronate (Fosamax®). Although she had a history of IBS, and alendronate as well as other oral bisphosphonates may cause gastrointestinal (GI) upset, alendronate has been found to effectively increase spine and hip bone density for women in early postmenopause (Rosen et al., 2005). In the Fracture Intervention Trial, alendronate reduced the rate of spine, hip, and wrist fractures by approximately 50% (Black et al., 2000).

P.C. received important information on correct administration of alendronate. She must take the medication in the morning on an empty stomach after 8 hours of fasting, with 8 ounces of water and wait 30 minutes before eating, drinking, or taking other medications, and she must remain upright during this entire 30-minute period. She was advised to report any GI upset to her nurse practitioner (NP). P.C. was scheduled for follow up in 1 month to discuss her nutrition, exercise, and other universal recommendations as well as how she is tolerating the alendronate. A repeat DXA scan would be performed in approximately 2 years to evaluate her overall response to treatment.

Individual Example 2

W.T. is an 83-year-old Caucasian woman who visits the NP-led osteoporosis clinic 6 weeks after surgery and initial rehabilitation in a skilled nursing facility following a hip fracture due to a fall at home. This visit was scheduled in accordance with a new initiative at her hospital to improve care following fragility fractures (Tosi, Gliklich, Kannan, & Koval, 2008). During her visit at the clinic, W.T. reported that she tripped and fell over a scatter rug in her apartment. Her daughter found her a few hours after the fall when she came for her daily visit. In addition to the current fracture, W.T. mentioned that she had fractured her humerus 3 years earlier from a ground-level fall as well. She was placed on alendronate at that time and was still taking it upon admission to the hospital.

In preparation for her hip surgery, she was admitted to the orthopedic unit, and prior to surgery was evaluated by a geriatrician. At that time, her laboratory results demonstrated a serum calcium of 8.8 mg/dL, glomerular filtration rate of 31, vitamin D 25 hydroxy of 24 ng/mL, and PTH of 72 pg/mL. She was started on vitamin D while in the hospital at a dose of 50,000 units twice per week for 6 weeks. The alendronate was discontinued due to stage 3 renal failure (Miller, Jamal, Evenepoel, Eastell, & Boonen, 2013).

When she was seen by the NP in the osteoporosis clinic, her laboratory results were reviewed again. By that time she had completed the high-dose vitamin D regimen and was placed on vitamin D3 2,000 IU per day. Plans were made to recheck her vitamin D level in 6 months. She was taught about taking calcium, 600 mg from a supplement and 600 mg from her diet. Calcium citrate was encouraged because it is more easily absorbed. W.T. was receiving in-home physical therapy for her hip; an order was written for the therapist to work with her on appropriate weight-bearing exercises and balance, to assess her home for fall hazards, and to make recommendations for avoidance of future falls based on the assessment results.

A decision was made to place W.T. on teriparatide (Forteo®), which is indicated for postmenopausal women who fail prior therapy and/or are at high risk of further fractures. It has been shown to increase BMD at the spine and hip and to decrease fracture risk by 50% to 65% (Neer et al., 2001). Because W.T. had a history of two fragility fractures, and sustained her current fracture while on alendronate, she fit the criteria. Teriparatide is a human recombinant PTH (PTH-1-34) that directly stimulates osteoblasts to improve bone formation. Currently, it is approved for use by the U.S. Food and Drug Administration for up to 24 months and is administered by a daily injection (Honig, Rajapakse, & Chang, 2013). Initially, W.T. was reluctant to inject herself but once she was taught how to perform the injection, she agreed to try it. Follow up was scheduled for 2 months to check on how she was doing with the Forteo injection. Another vitamin D level would be ordered as well. She would be followed every few months to assure compliance with the Forteo and adequate vitamin D level was being maintained.

Summary

Current treatments have the potential to significantly reduce the occurrence of fragility fractures among postmenopausal women. However, recognition of osteoporosis and provision of targeted treatment based on individual risk profiles is essential to prevent these fractures. Recent evidence suggests that health care providers are inadequately prepared for the emerging epidemic of osteoporosis and potential fragility fractures due to population aging (Bischoff-Ferrari, 2013). Furthermore, despite evidence that demonstrates major risk for a subsequent fracture among those who have sustained fractures, only 20% of those who sustain a fragility fracture receive treatment for osteoporosis (Andrade et al., 2003; Liu et al., 2013). There is an effort to improve this care. The American Orthopedic Association (AOA) is actively working to encourage orthopedic providers to recognize this problem and address it. Own the Bone is a program sponsored by the AOA that will assist in this process (Tosi et al., 2008). Nurses are in a unique position to raise awareness of the prevalence and impact of untreated osteoporosis and to intervene with clinical guideline recommendations and referrals for diagnostic evaluations and treatment. As shown in the individual examples above, postmenopausal women have diverse risks, varied treatment contra-indications, and different responses to treatments that require individualized care planning and follow up to maximize the effectiveness of treatment and minimize the potential for adverse outcomes.

References

  • American Society for Bone and Mineral Research. (2006). Primer on the metabolic bone diseases and disorders of mineral metabolism. Washington, DC: Author.
  • Andrade, S.E., Majumdar, S.R., Chan, K.A., Buist, D.S., Go, A.S., Goodman, M. & Gurwitz, J.H. (2003). Low frequency of treatment of osteoporosis among postmenopausal women following a fracture. Archives of Internal Medicine, 163, 2052–2057. doi:10.1001/archinte.163.17.2052 [CrossRef]
  • Bischoff-Ferrari, H. (2013). Fragility fractures: The future epidemic and its challenges. Skeletal Radiology, 42, 161–163. doi:10.1007/s00256-012-1549-4 [CrossRef]
  • Black, D.M., Thompson, D.E., Bauer, D.C., Ensrud, K., Musliner, T., Hochberg, M.C. & Cummings, S.R. (2000). Fracture risk reduction with alendronate in women with osteoporosis: The Fracture Intervention Trial. Journal of Clinical Endocrinology and Metabolism, 85, 4118–4224. doi:10.1210/jcem.85.11.6953 [CrossRef]
  • Cauley, J.A. (2013). Public health impact of osteoporosis. Journals of Gerontology. Series A, Biological Sciences and Medical Sciences, 68, 1243–1251. doi:10.1093/gerona/glt093 [CrossRef]
  • Cummings, S.R., Nevitt, M.C., Browner, W.S., Stone, K., Fox, K.M., Ensrud, K.E. & Vogt, T.M. (1995). Risk factors for hip fracture in white women: Study of Osteoporotic Fractures Research Group. New England Journal of Medicine, 332, 767–773. doi:10.1056/NEJM199503233321202 [CrossRef]
  • Fleisch, H. (2000). Bisphosphonates in bone disease: From the laboratory to the patient (4th ed.). San Diego, CA: Academic Press.
  • Garnero, P., Hausherr, E., Chapuy, M.C., Marcelli, C., Grandjean, H., Muller, C. & Delmas, P.D. (1996). Markers of bone resorption predict hip fracture in elderly women: The EPIDOS Prospective Study. Journal of Bone and Mineral Research, 11, 1531–1538. doi:10.1002/jbmr.5650111021 [CrossRef]
  • Honig, S., Rajapakse, C.H. & Chang, G. (2013). Current treatment approaches to osteoporosis–2013. Bulletin of the Hospital for Joint Diseases, 71, 184–188.
  • Kanis, J.A., Melton, L.J. III. , Christiansen, C., Johnston, C.C. & Khaltaev, N. (1994). The diagnosis of osteoporosis. Journal of Bone and Mineral Research, 9, 1137–1141. doi:10.1002/jbmr.5650090802 [CrossRef]
  • Liu, S.K., Munson, J.C., Bell, J.E., Zaha, R.L., Mecchella, J.N., Tosteson, A.N.A. & Morden, N.E. (2013). Quality of osteoporosis care of older Medicare recipients with fragility fractures: 2006 to 2010. Journal of the American Geriatrics Society, 61, 1855–1862. doi:10.1111/jgs.12507 [CrossRef]
  • McClung, M., Harris, S.T., Miller, P.D., Bauer, D.C., Davison, K.S., Dian, L. & Lewiecki, E.M. (2013). Bisphosphonate therapy for osteoporosis: Benefits, risks, and drug holiday. American Journal of Medicine, 126, 13–20. doi:10.1016/j.amjmed.2012.06.023 [CrossRef]
  • Miller, P.D., Jamal, S.A., Evenepoel, P., Eastell, R. & Boonen, S. (2013). Renal safety in patients treated with bisphosphonates for osteoporosis: A review. Journal of Bone and Mineral Research, 28, 2049–2059. doi:10.1002/jbmr.2058 [CrossRef]
  • National Osteoporosis Foundation. (2013). Clinician’s guide to prevention and treatment of osteoporosis. Retrieved from http://nof.org/hcp/clinicians-guide
  • Neer, R.M., Arnaud, C.D., Zanchetta, J.R., Prince, R., Gaich, G.A., Reginster, J.Y. & Mitlak, B.H. (2001). Effect of parathyroid hormone (1–34) on fractures and bone mineral density in postmenopausal women with osteoporosis. New England Journal of Medicine, 344, 1434–1441. doi:10.1056/NEJM200105103441904 [CrossRef]
  • North American Menopause Society. (2010). Management of osteoporosis in postmenopausal women: 2010 position statement of the North American Menopause Society. Menopause, 17, 25–54. doi:10.1097/gme.0b013e3181c617e6 [CrossRef]
  • Pacifici, R. (1996). Estrogen, cytokines, and pathogenesis of postmenopausal osteoporosis. Journal of Bone and Mineral Research, 11, 1043–1051. doi:10.1002/jbmr.5650110802 [CrossRef]
  • Pinkerton, J.V., Thomas, S. & Dalkin, A.C. (2013). Osteoporosis treatment and prevention for postmenopausal women: Current and future therapeutic options. Clinical Obstetrics and Gynecology, 56, 711–721. doi:10.1097/GRF.0b013e3182a9fb02 [CrossRef]
  • Raisz, L.G. (2005). Clinical practice. Screening for osteoporosis. New England Journal of Medicine, 353, 164–171. doi:10.1056/NEJMcp042092 [CrossRef]
  • Riggs, B.L., Khosla, S. & Melton, L.J. III. . (1998). A unitary model for involutional osteoporosis: Estrogen deficiency causes both type I and type II osteoporosis in postmenopausal women and contributes to bone loss in aging men. Journal of Bone and Mineral Research, 13, 763–773. doi:10.1359/jbmr.1998.13.5.763 [CrossRef]
  • Rosen, C.J., Hochberg, M.C., Bonnick, S.L., McClung, M., Miller, P., Broy, S. & de Papp, A.E. (2005). Treatment with once-weekly alendronate 70 mg compared with once-weekly risedronate 35 mg in women with postmenopausal osteoporosis: A randomized double-blind study. Journal of Bone and Mineral Research, 20, 141–151. doi:10.1359/JBMR.040920 [CrossRef]
  • Ross, A.C., Manson, J.E., Abrams, S.A., Aloia, J.F., Brannon, P.M., Clinton, S.K. & Shapses, S.A. (2011). The 2011 report on dietary reference intakes for calcium and vitamin D from the Institute of Medicine: What clinicians need to know. Journal of Clinical Endocrinology and Metabolism, 96, 53–58. doi:10.1210/jc.2010-2704 [CrossRef]
  • Seeman, E. (2013). Age- and menopause-related bone loss compromise cortical and trabecular microstructure. Journals of Gerontology. Series A, Biological Sciences and Medical Sciences, 68, 1218–1225. doi:10.1093/gerona/glt071 [CrossRef]
  • Tosi, L.L., Gliklich, R., Kannan, K. & Koval, K.J. (2008). The American Orthopaedic Association’s “Own the Bone” initiative to prevent secondary fractures. Journal of Bone and Joint Surgery America, 90, 163–173. doi:10.2106/JBJS.G.00682 [CrossRef]
  • U.S. Department of Health and Human Services. (2004). Bone health and osteoporosis: A report of the Surgeon General. Retrieved from http://www.surgeongeneral.gov/library/reports/bonehealth
  • Warriner, A.H. & Saag, K.G. (2013). Osteoporosis diagnosis and medical treatment. Orthopedic Clinics of North America, 44, 125–135. doi:10.1016/j.ocl.2013.01.005 [CrossRef]
  • Watts, N.B., Bilezikian, J.P., Camacho, P.M., Greenspan, S.L., Harris, S.T., Hodgson, S.F. & Petak, S.M. (2010). American Association of Clinical Endocrinologists medical guidelines for clinical practice for the diagnosis and treatment of postmenopausal osteoporosis. Endocrine Practice, 16(Suppl. 3), 1–37. doi:10.4158/EP.16.S3.1 [CrossRef]

Definition of Osteoporosis Based on Bone Mineral Density T-Scores and Fragility Fractures

Bone Density CategoryT-Score
Normal>1.0
Low bone density (osteopenia)−1.0 to −2.5
Osteoporosis>2.5
Severe or established osteoporosis>2.5 and 1 or more fragility fractures

Medications for Osteoporosis Treatment

DrugDoseClassificationContraindications
Alendronate (Fosamax®)70 mg PO weeklyBisphosphonateGFR <35; significant upper GI disorders
Risedronate (Actonel®)150 mg PO monthlyBisphosphonateGFR <35; significant upper GI disorders
Ibandronate (Boniva®)150 mg PO monthly 3 mg IV every 3 monthsBisphosphonateGFR <35; significant upper GI disorders (for oral preparation)
Zoledronic acid (Reclast®)5 mg IV once per yearBisphosphonateGFR <35
Teraparitide (Forteo®)20 mcg SQ everydayaAnabolic steroidHyperparathyroidism, radiated bone, open epiphyses
Denosumab (Prolia®)60 mg SQ everydayMonoclonal antibodyNone
Raloxifene (Evista®)60 mg PO everydaySelective estrogen receptor modulatorHistory of DVT or PE for postmenopausal women only

10.3928/00989134-20140204-01

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