Keywords

FormalPara Key Points
  1. 1.

    Bone health is particularly important in older women due to increased risk of osteoporosis.

  2. 2.

    Osteoporosis is primarily due to effects of aging and decrease in sex steroids.

  3. 3.

    Tobacco and alcohol use can increase risk of osteoporosis.

  4. 4.

    Osteoporosis often presents with pathologic fractures of the vertebrae, hip, or radius.

  5. 5.

    Routine screening for osteoporosis is recommended at age 65 or earlier in someone with a fragility fracture or other risk factors.

  6. 6.

    Calcium and vitamin D supplementation are recommended in postmenopausal women.

  7. 7.

    Weight-bearing and resistance exercises are key components of bone health.

  8. 8.

    Bisphosphonates are effective first-line treatments for osteoporosis.

FormalPara Case

The next patient in your clinic is Ester, a 67-year-old woman with history of chronic kidney disease (CKD) stage 3A, hypertension, chronic obstructive pulmonary disease (COPD), and acid reflux, who is coming in for an annual exam after not being seen for several years. She quit smoking cigarettes 10 years ago and takes lisinopril, inhaled fluticasone, and omeprazole. She walks twice per week and recently started a plant-based diet. When you ask if she has any concerns, she says, “My older sister recently fractured her hip, and I am worried that I might have osteoporosis.”

Definitions

Osteoporosis is a disease characterized by low bone density and disordered architecture of the bones.

Osteopenia refers to bones that are weakened but not as severely as in osteoporosis.

Epidemiology and Risk Factors and Pathogenesis

Epidemiology

Osteoporosis is the most common bone disorder seen in postmenopausal women. Osteoporosis is characterized by low bone density and disordered bone architecture and predisposes to fractures. Latest estimates suggest that close to 10 million Americans have osteoporosis and an additional 43 million have osteopenia [1]. Worldwide, it is estimated that one in three women over age 50 will experience an osteoporotic fracture during their lifetime [2].

The 44 million people in the USA with osteoporosis and osteopenia comprise 55% of people over 50 years of age [2].

Risk Factors and Pathogenesis

The biggest risk factor for osteoporosis is low bone density. Bone density is determined by peak bone density and rate of bone loss. Peak bone mass is based on genetics and nutritional intake and is achieved by the second or third decade of life and starts to slowly decline around age 30 (Fig. 3.1) [3, 4]. Bone formation is balanced with bone remodeling until menopause when the process becomes uncoupled, causing a rapid decline in bone density.

Fig. 3.1
figure 1

Bone growth and loss: bone mass starts to decline around age 30, leading to skeletal changes, including kyphosis [5]

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A recent cohort study of almost 6400 people measured bone density tests every 5 years between ages 10 and 25 and found that later age of puberty was correlated with lower peak bone density [6].

Other risk fractures for osteoporosis and fracture can be divided into two groups: fixed risk factors and medical or lifestyle factors (Table 3.1). Osteoporosis is more common in White and Asian women than in African American women.

Table 3.1 Fixed risk factors for osteoporosis
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Pathophysiology

Not excited about reading about pathophysiology? Check out this Osmosis video for a helpful 9-minute summary of osteoporosis pathophysiology. https://www.youtube.com/watch?v=jUQ_tt_zJDo&vl=ru [7].

Osteoporosis can result from primary and secondary causes. Primary osteoporosis in women is due to bone loss as a result of two things: aging and decrease in sex steroids. During premenopausal years, bone remodeling by osteoblasts creates strong bones, but over time bone resorption from osteoclasts outpaces bone formation by osteoblasts leading to decreased bone formation.

Additionally, aging results in deterioration of the bone microarchitecture and decreased bone mass through bone-intrinsic factors such as oxidative stress, mitochondrial dysfunction, DNA damage, and lipid peroxidation, and also through bone-extrinsic factors such as changes in the immune system and ovaries [3, 4].

Sex hormones including estrogen and androgens help to maintain bone homeostasis by keeping a balance between bone resorption and remodeling. When sex hormones decrease during menopause, this balance becomes off and bone resorption increases [3].

Secondary causes of osteoporosis include medical conditions and use of substances such as tobacco, alcohol, and medications that increase bone resorption and decrease calcium absorption (Tables 3.2 and 3.3).

Table 3.2 Medical conditions that result in secondary osteoporosis [4, 8]
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Table 3.3 Medications that increase risk of osteoporosis [10, 11]
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Even Subclinical Hyperthyroidism Increases Fracture Risk [9]

A large meta-analysis (total of over 70,000 participants) found that people with subclinical hyperthyroidism (especially among people with a TSH <0.10 mIU/L) were at higher risk of hip and other fractures. This should be considered when assessing overall risk.

How Glucocorticoids Impact Bone Health

Excess glucocorticoids affect osteoblasts, osteoclasts, and osteocytes by suppressing osteoblastogenesis, which stimulates apoptosis of osteoblasts and osteocytes and increases the lifespan of osteoclasts, leading to increased bone destruction and decreased bone formation [3].

Case (Continued)

What Are Ester’s Risk Factors for Osteoporosis?

Age > 65, female, family history of osteoporotic fracture, chronic conditions (CKD, COPD), history of tobacco use, and medications (PPI).

Case (Continued)

Clinical Presentation

When you ask more about why Ester is worried about osteoporosis, she discusses her sister’s recent fracture and also mentions that she has been having intermittent knee and shoulder pain over the past year and wonders if this might be due to osteoporosis.

Myth Buster

Some patient assume they have joint pain caused by osteoporosis and others assume they do not have osteoporosis if they do not have any symptoms. Both are false.

Osteoporosis and osteopenia are asymptomatic until a fracture occurs. Fragility or pathologic fractures are the most common presentations of osteoporosis and are fractures that occur spontaneously or as a result of minor trauma such as a fall from standing height that normally would not result in a fracture. The most common pathologic fracture sites are the vertebrae, femoral neck, and distal radius [12, 13].

The most clinically significant fractures are hip fractures, but vertebral fractures can cause chronic pain and disability as well (Table 3.4). Hip fractures are associated with significant excess mortality and disability. Only 40% of people with a hip fracture regain their pre-fracture level of independence and up to 20% will never leave a long-term care facility after a fracture [10].

Table 3.4 Effects of vertebral fractures
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Screening and Diagnosis

Case (Continued)

Ester has never had osteoporosis screening but would like to be screened due to her family history. Does she qualify for screening, and if so, what screening options would you recommend for her?

Screening

Short and Sweet: Who to Screen for Osteoporosis?

All women >65 years old and all women >50 years old who sustain a fragility fracture or whose osteoporosis risk using the Fracture Risk Assessment Tool (FRAX) is equal to that of a 65-year-old woman.

Osteoporosis screening with a direct bone density measurement should be considered in all women aged 65 and older regardless of risk factors according to the United States Preventive Services Task Force (USPSTF) [14]. These guidelines are based on evidence that though there is a rapid loss of bone mineral density (BMD) in the lumbar spine in all women after menopause, the risk of fracture does not begin to increase exponentially until age 70–79 [15].

There is less clear evidence regarding screening younger postmenopausal women for osteoporosis, in particular, which risk factors to consider and at what age to begin screening. A 2010 comparison review of screening instruments demonstrated that most include similar considerations and are generally equivalent in predicting fracture risk, regardless of the instrument complexity [16]. The USPSTF suggests using the FRAX to determine a patient’s risk for osteoporosis and consider screening women at an earlier age who have a 10-year fracture risk that is equal to a 65-year-old white woman without additional risk factors (8.4% for a woman of mean height and weight) in conjunction with a shared decision-making conversation with the patient [14, 16]. The American Association of Clinical Endocrinologists (AACE)/American College of Endocrinology (ACE) recommends evaluating all premenopausal women age ≥ 50 utilizing a tool such as the FRAX or Osteoporosis Self-assessment Tool (OST) [17].

Check out the interactive FRAX at this link: https://www.sheffield.ac.uk/FRAX/ [18]

What is clear is that all women who sustain a “fragility fracture,” a fracture that occurs in the absence of significant trauma, over age 50 should be evaluated with a bone density measurement to evaluate for osteoporosis [11].

Screening Methods

Short and Sweet: How to Screen?

Dual energy X-ray absorptiometry (DEXA) scan is the gold standard for screening.

Screening Methods (Table 3.5)

DEXA is the gold standard for bone mineral density (BMD) measurement as it directly measures the bone density at the vertebra and femur. In the DEXA scan, energy from two low-dose X-ray beams passes through and is absorbed by bones, and the energy that is not absorbed is detected on the other side of the body. Bones that are denser absorb more energy so less energy is detected. The amount of radiation exposure is similar to that from a single chest X-ray [19].

Table 3.5 Screening methods for osteoporosis
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Watch this video to understand how a DEXA scan works: https://www.youtube.com/watch?v=7EkK1oMK5A8 [20]

Peripheral DEXA (pDEXA) is similar to central DEXA but measures the BMD at peripheral sites. The measurement devices are portable, which may increase access, and limited data have corroborated its efficacy in identifying osteoporosis. However, it has not been correlated with central DEXA to validate treatment thresholds [14].

Calcaneal ultrasound predicts osteoporosis-related fracture and is generally more portable and less expensive than DEXA. However, it does not directly measure the BMD, nor does it correlate strongly with DEXA, which is the foundation for medication treatment thresholds that have shown efficacy [14].

Most national guidelines do not include vertebral imaging (plain films) as a standard recommendation for osteoporosis screening. The National Osteoporosis Foundation (NOF) suggests to consider plain films to screen for occult vertebral fractures in certain populations: (1) women over age 70 with normal T-score; (2) women over age 65 with osteopenia; and (3) postmenopausal women over age 50 with risks (fragility fracture, loss of height, or glucocorticoid treatment) [11].

What About Labs?

Biochemical markers of bone remodeling are not a standard screening recommendation. These markers may be useful in high-risk groups or in monitoring for response to treatment; however, further evidence is needed [21]. Screening for secondary causes of osteoporosis with tests like serum calcium, vitamin D, creatinine, glucose, parathyroid hormone, and thyroid stimulating hormone may be appropriate in postmenopausal women with risk factors such as high-risk medications, strong family history of osteoporosis, and history of fragility fracture.

There are minimal data regarding the harms of osteoporosis screening; these may include radiation exposure, depending on the method, and opportunity cost [14]. There is one study demonstrating that screening does not impact anxiety levels or quality of life [22].

Diagnosis

Bone density results are reported with a T-score, which indicates bone density relative to the bone density of a healthy 30-year-old woman. Normal bone density is above −1 and low bone density is −1 and below.

Osteoporosis: Fragility fracture or T-score < −2.5 at the lumbar spine, femoral neck, or total femur (use the lowest T-score).

Osteopenia: Low normal bone density defined as T-score between −1 and −2.5 at the lumbar spine, femoral neck, or total femur (use the lowest T-score).

Case (Continued)

Ester elects to have a DEXA scan. Her results show that her lowest T-score is at her femoral neck and is −2.0 and she has a 10-year probability of hip fracture of 1% and 10-year probability of major osteoporotic fracture of 10%. She is diagnosed with osteopenia and asks, “When do I need to have this test repeated?”

How Often Should Women Be Screened for Osteoporosis?

The optimal frequency of bone density measurement has not been determined, although two large studies demonstrated minimal additional benefit in predicting future fractures with a repeat screening at either 4 or 8 years for women not treated with bisphosphonates [23, 24]. For patients on medication therapy for osteoporosis, the National Osteoporosis Foundation recommends BMD testing 1–2 years after starting treatment and then every 2 years [12].

Prevention and Management

Prevention and Lifestyle Treatments

Case (Continued)

Ester is relieved that she does not have osteoporosis but is worried about her osteopenia and wants to do everything possible to prevent it from progressing to osteoporosis. She would like to avoid taking medication if possible but is eager to lead a healthy lifestyle. What options you would suggest to Ester?

Primary prevention of osteoporosis begins with achieving adequate peak bone density in adolescence and early adulthood through optimal nutrition and physical activity. Later in adulthood, primary prevention centers around maintaining bone mass and healthy skeletal microarchitecture. Strategies include adequate nutrition, and weight-bearing and resistance exercises (Table 3.6). Though the data are mixed, the National Osteoporosis Foundation recommends adequate calcium and vitamin D intake in persons over 50 years of age. Standard recommendations for most postmenopausal women with osteoporosis include a total calcium intake of 1000–1500 mg/day and a total vitamin D intake of 600–800 IU per day through diet, supplements, or both [25].

Table 3.6 Lifestyle preventive treatments for osteoporosis
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When Should You Offer Preventive Medications to Patients with Osteopenia?

Preventive medications may be considered in people with osteopenia (T-score between −1.0 and −2.5 at the femoral neck or lumbar spine) and a 10-year probability of a hip fracture ≥3% or a 10-year probability of a major osteoporosis-related fracture ≥20% based on the US adapted WHO algorithm [11].

Diet

A healthy, well-balanced diet is essential to developing and maintaining healthy bone mineral density and preventing fractures. In postmenopausal women, there is a positive association between higher fruit and vegetable intake and higher bone mineral density with less loss of bone mineral density over time. Fruits and vegetables are important sources of multiple nutrients for bone health, including calcium carotenoids, lycopene, vitamin K, potassium, and magnesium, all of which have demonstrated an inverse relationship with bone turnover, a positive relationship with bone density, or an inverse relationship with fracture risk [26].

The Framingham osteoporosis study demonstrated that men and women with diets rich in fish (>3 servings per week) over 4 years experienced an increase in bone mineral density, which was not observed in people with only low to moderate fish intake. These findings have been corroborated by multiple cross-sectional cohort studies of bone mineral density in postmenopausal Chinese women as well [26].

Milk and yogurt may have a protective effect against hip fractures, and this effect may be in part mediated by a positive effect of these foods on bone mineral density. Other dairy foods do not appear to affect fracture risk [26].

Calcium and Vitamin D

The effect of calcium and vitamin D on fracture risk is controversial [26]. Calcium is stored in the bones and adequate calcium stores are essential to healthy bone microarchitecture [27]. Vitamin D3 is necessary for the absorption of calcium from the gut [27]. In a randomized controlled trial of more than 36,000 postmenopausal women, 1000 mg of elemental calcium and 400 international units of vitamin D daily failed to demonstrate a fracture benefit. However, subgroup analysis suggests that women over 60 and women who were adherent to the regimen of calcium and vitamin D did suffer fewer fractures. There are data from populations of institutionalized elderly and elderly people with low dietary calcium and vitamin D intake that corroborate these findings. Therefore, the National Osteoporosis Foundation recommends calcium and vitamin D supplementation in persons over 50 years of age [11]. Standard recommendations for most postmenopausal women with osteoporosis include a total calcium intake of 1000–1500 mg per day, and a total vitamin D intake of 600–800 IU per day through diet, supplements, or both [25].

Case (Continued)

When you discuss calcium and vitamin D with Ester, she says, “I’ve heard that calcium can increase my risk of heart disease. Is that true?”

Calcium and Cardiovascular Disease

There is no evidence to date that dietary calcium increases the risk of coronary artery calcification or cardiovascular events. A list of calcium-rich foods can be found here: https://www.iofbonehealth.org/osteoporosis-musculoskeletal-disorders/osteoporosis/prevention/calcium/calcium-content-common-foods [28]

There is some evidence that if someone is taking supplemental calcium and total calcium intake exceeds 1400 mg per day, there may be an increased risk of coronary artery calcification and myocardial infarction [29]. Experts agree that obtaining adequate calcium from food is the preferred way to promote optimal bone and cardiovascular health [29, 30].

Exercise

Exercise decreases the risk of falls and fractures through improved bone mineral density, improved balance, and decreased risk of falls. The National Osteoporosis Foundation recommends a program of weight-bearing and resistance exercises to prevent falls and fractures, and a sample exercise regimen is available on the NOF website: https://www.nof.org/preventing-fractures/exercise-to-stay-healthy/ [31].

Nonweight-bearing high-force resistance exercises such as strength training for the lower limbs have the most robust evidence for BMD of the femur neck. For BMD of the spine, combined programs comprising more than one exercise type show the most benefit [32].

Tai Chi shows a protective effect against falls, decreasing the risk of falling at least once, and decreasing the rate of falls [33]. Taking part in yoga has been shown to decrease the risk of lower limb fractures [34]. Yoga programs specific to patients with osteoporosis are available.

Smoking Cessation

First- and second-hand tobacco smoke have a negative effect on bone mass. Tobacco smoke directly affects osteogenesis and bone angiogenesis. Additionally, tobacco smoke mediates indirect effects on bone tissue through alteration of body weight, parathyroid hormone–vitamin D axis, adrenal hormones, sex hormones, and increased oxidative stress. These deleterious effects on skeletal health are largely reversible with tobacco cessation [35].

The Centers for Disease Control and Prevention (CDC) has a smoking cessation website specifically for adults aged 60 and older.

Alcohol Consumption

The National Osteoporosis Foundation recommends screening for and treating excessive alcohol use (>2 alcoholic beverages per day for women) [11]. Alcohol use in moderation may have a protective effect on bone mineral density. In one study, compared to no consumption, low to moderate alcohol consumption was associated with a lower risk of hip fractures, particularly with red wine consumption among women [36].

Fall Prevention

Exercise, personalized risk assessment and intervention, and home safety evaluation and modification performed by an occupational therapist all reduce the risk of falls. In people with vitamin D deficiency, vitamin D supplementation may reduce the risk of falls. There is no role for vitamin D supplementation in people with normal vitamin D levels for prevention of falls. Evidence is mixed for the review and management of psychotropic medication for reducing falls. The gradual withdrawal of psychotropic medications may have a positive impact on falls, though evidence for this is most robust when prescribers are supported by drug management protocols [37].

The Centers for Disease Control and Prevention (CDC) has a helpful falls prevention toolkit (Stopping Elderly Accidents, Deaths, and Injuries) for healthcare providers https://www.cdc.gov/steadi/index.html. Many community organizations offer evidence-based falls prevention programs for older adults: the National Council on Aging provides information about how to find these programs in your community https://ncoa.org/ncoa-map.

Pharmacologic Treatment

Case (Continued)

Ester opts to increase calcium in her diet, start calcium and vitamin D supplementation, and introduce Tai Chi and strength training into her weekly routine. She is thankful that she quit smoking 10 years ago. Ester’s sister Lucy, who is 70 and recently broke her hip after tripping over a rug in her home, is also your patient and comes to see you for a hospital follow-up visit. She had a normal DEXA scan at age 65 and had not had a repeat scan. You order a DEXA scan, which shows osteoporosis. What treatment would you recommend for Lucy?

Candidates for Pharmacologic Therapy

Postmenopausal women and men aged 50 and older presenting with any of the following should be considered for treatment:

  1. 1.

    A hip or vertebral fracture in a patient with osteopenia or osteoporosis.

  2. 2.

    T-score ≤−2.5 at the femoral neck, total hip, or lumbar spine.

  3. 3.

    Low bone mass/osteoporosis (T-score between −1.0 and −2.5 at the femoral neck or lumbar spine) and a 10-year probability of a hip fracture ≥3% or a 10-year probability of a major osteoporotic fracture ≥20% [18].

Pharmacologic agents for the treatment of osteoporosis have been shown to improve BMD and reduce the risk of fractures. These can be classified as antiresorptive, slowing osteoclast-mediated bone resorption, or anabolic, stimulating osteoblasts to form new bone [11].

Bisphosphonates

These drugs are FDA approved for the prevention and treatment of osteoporosis, and they are the most prescribed class of drugs for these indications (Table 3.7). They work by inhibiting bone remodeling.

Table 3.7 Bisphosphonate indications, dosing, and administration
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Use of bisphosphonates should be limited to persons who have an estimated creatinine clearance greater than 35 mL/min. Symptomatic hypocalcemia can develop in patients with low vitamin D levels who are treated with bisphosphonates [25]. Therefore, the National Osteoporosis Foundation recommends screening for and correcting vitamin D deficiency in conjunction with bisphosphonate therapy. The therapeutic target for vitamin D supplementation is 30 ng/mL (75 nmol/L), and maintenance dosing should continue to maintain this level [11].

Case (Continued)

You and Lucy decide to initiate bisphosphonate therapy for Lucy. When should you start bisphosphonate therapy in a patient with fracture?

Initiation of Bisphosphonate Therapy in a Patient After Fracture

It is best to wait 4–6 weeks after a fracture before starting bisphosphonate therapy.

Minor gastrointestinal irritation may occur with oral bisphosphonate therapy; this side effect may be minimized by adherence to dosing instructions. It is estimated that less than 40% of persons who are prescribed oral bisphosphonates are still taking them after 1 year. Intravenous preparations with less frequent dosing intervals may therefore be preferred [25].

Rarely, atypical femur fractures and osteonecrosis of the jaw are observed with bisphosphonate therapy. The risk of these complications increases with protracted (>5 years) use. Patients with atypical femur fractures may present with new thigh or groin pain and patients on bisphosphonate therapy should be screened for these symptoms, with bilateral femur X-rays as part of the initial evaluation of these symptoms [11].

Medication-related osteonecrosis of the jaw (MRONJ) is defined as exposed maxillofacial bone for greater than 8 weeks in patients with known exposure to an offending medication and no history of radiation or metastases to the jaw. This primarily occurs in patients on high-dose bisphosphonates for cancer therapy. Denosumab and other antiresorptive agents have also been implicated in the development of MRONJ. Physical examination may reveal exposed bone with no other symptoms. MRONJ requires dental consultation for further evaluation and management [38].

Estrogen

Estrogen treatment affects osteocytes, osteoclasts, and osteoblasts, causing inhibition of bone resorption and maintenance of bone formation [25]. Estrogen is FDA approved for osteoporosis prevention [11]. In women who have not had a hysterectomy, estrogen is administered with progesterone to prevent endometrial cancer [11]. In the large multicenter Women’s Health Initiative trials, estrogen significantly reduced the incidence of new vertebral, nonvertebral, and hip fractures. Estrogen is not recommended as first-line therapy for osteoporosis prevention, in part due to concerns about nonskeletal risks associated with estrogen use including breast cancer and coronary, cerebrovascular, and thrombotic events [25].

SERMs

Selective estrogen-receptor modulators (SERMs) activate tissue receptors for estrogen that affect bone turnover. Raloxifene is a SERM with FDA approval for the treatment of osteoporosis. It inhibits bone resorption, increases spine BMD, and decreases the risk of vertebral fractures by 30%. Raloxifene has no effect on the risk of hip or other nonvertebral fractures [25]. Like estrogen, Raloxifene increases the risk of deep vein thrombosis. Hot flashes and leg cramps are other commonly observed side effects [11].

Estrogen/SERM

Conjugated estrogens/bazedoxifene is a combination of estrogen and a SERM approved by the FDA to prevent osteoporosis after menopause. This drug significantly increases mean lumbar spine BMD after a year of therapy as compared to placebo in women who have been postmenopausal between 1 and 5 years. This drug also significantly increases total hip BMD [11].

Denosumab

Denosumab is a human monoclonal antibody that inhibits bone resorption by inhibiting osteoclasts [25]. Denosumab is approved by the FDA for the treatment of osteoporosis in postmenopausal women at high risk of fracture [11]. This drug lowers risk of vertebral fractures by 68%, hip fractures by 40%, and other nonvertebral fractures by 20% as compared to placebo. It can be used in women with compromised renal function. As with bisphosphonates, rare cases of atypical femur fractures and osteonecrosis of the jaw have been observed with denosumab treatment [25].

Calcitonin

Calcitonin nasal spray is FDA approved for women who are at least 5 years postmenopausal when other osteoporosis treatments are not appropriate. Calcitonin reduces vertebral fracture occurrence by about 30% in those with prior vertebral fractures but has not been shown to reduce the risk of nonvertebral fractures. Calcitonin may cause rhinitis, epistaxis, and allergic reactions, particularly in those with a history of allergy to salmon. Calcitonin may be associated with malignancy, and need for this therapy should be frequently reassessed [11].

Teriparatide

Teriparatide (recombinant human parathyroid hormone [rhPTH]) stimulates osteoblastic bone formation to increase bone mass and improve bone architecture [39]. Teriparatide is FDA approved for the treatment of osteoporosis in men and postmenopausal women with high risk of fracture, including those with a history of glucocorticoid use [40]. Teriparatide is administered daily by self-injection for 24 months [39]. This drug lowered the risk of vertebral fractures by 65% and nonvertebral fractures by 53% in a large randomized placebo-controlled trial [41]. These benefits persisted beyond the treatment interval. In clinical trials, rare cases of osteosarcoma were observed, though no causal link has been established [39].

Duration of Therapy

The recommended duration of therapy for bisphosphonates is 3–5 years, after which time a 3–5 year drug holiday is recommended because the potential for additional therapeutic effect wanes and the risk of osteonecrosis of the jaw and atypical femur fractures increases. The benefits of bisphosphonate therapy persist for a few years after discontinuation of therapy. The effects of nonbisphosphonate therapies attenuate rapidly after therapy discontinuation, with the exception of teriparatide [11].

Case (Continued)

Lucy takes alendronate for 5 years, with improvements seen on interval DEXA scans. Five years after finishing treatment, at age 80, she has a repeat bone density scan, which shows worsening of her osteoporosis. Should she restart the medication?

There is not clear evidence or guidelines about when to restart bisphosphonates after a drug holiday. Patients with risk factors such as decrease in BMD, new fracture, or other clinical risk factors for fracture who were previously treated may benefit from restarting therapy if there has been persistent bone loss (about 5%) on at least two DEXA scans taken at least 2 years apart. Additionally, if a patient with osteoporosis was treated and had a 3–5 year holiday with documented improvement from therapy and no history of fractures, you can also consider restarting therapy [42].

Bone health can have a significant impact on the lives of older women. Healthy bones can pave the way for a healthy, active lifestyle whereas osteoporosis can lead to significant morbidity. Thus, routine bone health risk assessment and screening and discussion of preventive and therapeutic treatment options are very important in order to maximize bone health and quality of life.