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Musculoskeletal

Osteoporosis

Verified · Sep 2026

Osteoporosis is a systemic skeletal disease of low bone mass and distorted microarchitecture that leaves bone fragile — diagnosed by a DXA T-score of −2.5 or lower, or by a fragility fracture of the hip or spine regardless of the T-score.

The disorder behind the T-score, the DXA scan, FRAX, the upright-for-30-minutes bisphosphonate rule, the dental exam before the first dose, and the height check that finds a fracture nobody felt.

What’s going wrong in the body

The normal physiology, where it fails, and why the body’s compensation backfires.

01 Bone is a tissue in constant turnover — and RANKL is the switch

Bone is not scaffolding; it is a tissue being demolished and rebuilt continuously by three cell types. Osteoblasts form osteoid matrix, osteoclasts digest calcified bone matrix, and osteocytes regulate overall bone homeostasis. Osteoporosis is not a disease of "weak bone" in the abstract — it is an imbalance in which resorption outpaces formation, or, in patient-level terms, the condition that occurs when "more bone is broken down than replaced."

The control system is the RANKL axis, and it is worth learning because every major drug targets it. Osteoblasts release receptor activator of nuclear factor kappa-B ligand (RANKL), which "acts upon RANK receptors on osteoclast precursors, stimulating active resorption." The brake is osteoprotegerin, which "is released from osteocytes and binds to RANKL to inhibit its function, leading to an inhibition of bone resorption." The balance between those two molecules sets how fast bone is dismantled.

Two clinical facts fall directly out of that mechanism. First, denosumab is a manufactured version of the brake — a "total human IgG2 monoclonal antibody that binds to… RANKL" and "competitively inhibits its binding to… RANK." Second, and more common on the ward, glucocorticoids work by removing it: they act through glucocorticoid receptors causing "a decrease in osteoprotegerin (OPG) and osteocalcin levels with an unopposed RANKL activity." A patient on long-term prednisone has had the brake taken off the same system denosumab exists to hold down.

The RANKL axis: osteoblasts drive resorption through RANKL and restrain it through osteoprotegerin. Denosumab adds a manufactured brake; glucocorticoids remove the natural one.

02 Peak bone mass, then the estrogen cliff

Everything after the third decade is a withdrawal from an account that has stopped taking deposits. About 50% of peak bone mass is attained during adolescence, the peak arrives in the third decade, and 60% to 80% of it is genetically predetermined. Peak mass is 10% lower in females than in males, and the payoff for building more of it is large: an increase in peak bone mass in children and adolescents "can reduce the risk of an osteoporotic fracture during adulthood by nearly 50%."

Menopausal bone loss is a cliff, not a slope. Estrogen decline "leads to rapid acceleration of bone loss starting the year before menopause." The steepest fall is about 5% annually in the first year post-menopause, easing to 1% to 1.5% per year afterwards, with an average of 10% to 12% lost at the spine and hip across the menopausal transition — and by age 80, roughly 30% of peak bone mass is gone. Over a lifetime, women lose 50% of trabecular and 35% of cortical bone.

One structural detail explains why the loss is harder to reverse in women: with aging, "trabecular perforations and loss occur in women, compared to trabecular thinning, but not loss, in men." A thinned strut can be thickened again; a perforated one has lost its connection to the lattice and does not come back, which is why architecture — not just density — is what the word "osteoporosis" is describing. Running alongside this is sarcopenia: from the fourth decade, 3% to 5% of muscle mass is lost per decade, worsening to 1% to 2% annually after age 50. Weaker muscles mean more falls, and a fall onto weakened bone is the fracture. Bone loss and muscle loss are one clinical problem, not two.

The bone-mass lifecourse: a genetically capped peak in the third decade, an accelerated loss beginning a year before menopause, and architecture that perforates rather than merely thins — with sarcopenia supplying the fall.

03 Why vertebrae break first and hips break later

The two classic patterns of osteoporosis are not arbitrary — they follow the ratio of trabecular to cortical bone at each site. Type 1 (postmenopausal) osteoporosis occurs "approximately 10 to 15 years following menopause, in the typical age group of 50 to 70 years," affects up to 25% of women in early menopause, is caused by estrogen deficiency, and produces predominantly trabecular bone loss. The vertebrae are 75:25 trabecular to cortical — so they are where an estrogen-driven, trabecular-dominant process shows up first.

Type 2 (senile) osteoporosis occurs after age 70 from "low turnover," the "result of gradual trabecular and cortical bone loss" and predominantly cortical involvement. The femoral neck is 30:70 trabecular to cortical — the reverse ratio — which is why hip fractures dominate the later decades. The same disease, read through two different bone compositions, produces two different fracture epidemics a couple of decades apart.

A third pattern matters most for men. Secondary osteoporosis — bone loss or fragility fracture in a person who has an identifiable cause — accounts for 30% of women but 50% to 80% of men with osteoporosis. In a man with osteoporosis, a secondary cause is more likely than not, and must be actively hunted rather than assumed absent. The lab signal that prompts the hunt is the Z-score: a value of −2.0 or lower is below the expected range for that age and should trigger a secondary-cause workup.

04 The first fracture is the diagnosis — and the warning

Osteoporosis is silent until it breaks something. The patient-facing wording is worth quoting exactly: "Osteoporosis is called a 'silent' disease because it doesn't usually cause symptoms. You may not even know you have the disease until you break a bone." That single sentence is why this disorder is found by screening rather than by symptom review, and why "the patient feels fine" carries no information.

Once a fragility fracture happens, the risk of the next one changes permanently. A prior fracture after menopause carries roughly a two-fold increase versus age- and BMD-matched peers, with risk that "persists for up to 10 years, with the highest risk being in the first 2 years." An existing vertebral fracture confers a five-fold increase in subsequent fracture risk, and the number that lands with patients is this one: a 65-year-old with one vertebral fracture has a 1 in 4 chance of another within 5 years, reduced to 1 in 8 with treatment. "A single vertebral fracture dramatically increases the risk of subsequent vertebral and other osteoporotic fractures."

And yet the cascade keeps running, because nobody explains it. The sourced education gap is stark: 35% of patients are unaware osteoporosis caused their fracture, nearly 50% blamed the fracture on "clumsiness," and over 50% are unaware that one fracture increases the risk of the next. A vertebral fracture is also easy to miss clinically — "many VCFs remain asymptomatic or present with mild, tolerable discomfort," with roughly a third found incidentally on radiographs. This is the strongest argument in the whole disorder for deliberate post-fracture teaching: the fracture is not bad luck, it is a diagnosis, and it predicts the next one.

The fracture cascade: the first fragility fracture doubles future risk, a vertebral fracture multiplies it five-fold, and a hip or vertebral fracture alone justifies treatment whatever the T-score says.

Causes & risk factors

Modifiable factors are teaching targets — the patient can act on them.

Advancing age — 85% of nursing home residents over 80 have osteoporosis Female sex and postmenopausal status — about 80% of the 10.3 million affected Americans are women, including 21.2% of women over 50 worldwide A prior fragility fracture — roughly a two-fold increase in future risk, and a five-fold increase if the prior fracture was vertebral Family history — nearly 20% report a positive family history, and maternal hip fracture raises offspring risk Low body weight — under 127 lbs or BMI under 21 kg/m² increases fracture risk and is a named screening trigger modifiable Smoking — lower average BMD plus a 30% increased fracture risk independent of BMD; cessation raises BMD and lowers fracture risk modifiable Alcohol — more than 2 units daily weakens BMD in women; more than 3 units daily brings a 38% increase in major osteoporotic and 68% increase in hip fractures modifiable Physical inactivity and immobility — moderate exercise improves BMD, and the benefit is lost if activity stops modifiable Low calcium and vitamin D intake — average US calcium intake is only 600 to 800 mg/day, well below the recommended range modifiable Glucocorticoids — the commonest drug cause; fracture risk is assessed at ≥ 2.5 mg prednisone equivalent for ≥ 3 months (American College of Rheumatology, via StatPearls) modifiable Other bone-losing medications — depot medroxyprogesterone, antiepileptics, SSRIs, proton pump inhibitors, thiazolidinediones, aromatase inhibitors, androgen deprivation therapy, heparin modifiable Endocrine secondary causes — primary hyperparathyroidism, Cushing syndrome, hyperthyroidism, hypogonadism and premature ovarian insufficiency, diabetes mellitus Gastrointestinal and rheumatologic causes — inflammatory bowel disease, celiac disease, chronic liver disease, rheumatoid arthritis, cystic fibrosis, COPD Renal and hematologic causes — chronic kidney disease–mineral bone disorder, idiopathic hypercalciuria, multiple myeloma and monoclonal gammopathy

Signs & symptoms

Each finding tied to the mechanism that produces it — and the triage it calls for.

Nothing at all — osteoporosis is a "silent" disease early Expected
Why: "You may not even know you have the disease until you break a bone." There is no pain, no stiffness and no warning from the bone itself while density and architecture are being lost. This is why screening, not symptom review, is what finds it — and why "I feel fine" is not reassurance.
Acute back pain after minimal or no trauma, worse on movement and standing Hold & notify
Why: The hallmark symptom of a vertebral compression fracture — "substantial pain, impaired mobility, loss of independence, and significantly reduced quality of life." New focal back pain in an older adult, especially one on glucocorticoids, is a fracture until it has been imaged.
Back pain that is nocturnal, at multiple skeletal sites, or paired with unexplained weight loss or a cancer history Report immediately
Why: These are the sourced red flags that take the workup out of simple osteoporosis and into investigation for neoplastic causes, particularly multiple myeloma. Serum protein electrophoresis with light chains belongs in the workup, and MRI distinguishes an osteoporotic from a malignant fracture by marrow signal and soft-tissue extension.
Height loss of 1.5 inches or more, and kyphotic posture Hold & notify
Why: Accumulated vertebral collapse made visible — with progressive vertebral collapse, patients "may often show a kyphotic posture, colloquially known as the ‘Dowager’s Hump’." Height loss of ≥ 1.5 inches indicates the need for vertebral imaging, which is why routine height measurement is recommended at each encounter. It is the one bedside measurement that detects a fracture the patient never felt.
A vertebral fracture found incidentally on an unrelated radiograph Hold & notify
Why: "Many VCFs remain asymptomatic or present with mild, tolerable discomfort," and about a third are diagnosed radiographically. One-quarter of women aged 50 and over have at least one, rising from about 3% under 60 to about 20% at 70 and above. An incidental vertebral fracture is a diagnosis of osteoporosis and an indication to treat.
Fracture at the thoracolumbar junction — T12 to L2 Hold & notify
Why: 60% to 75% of vertebral compression fractures occur at T12 to L2, with another 30% at L2 to L5. That is where the relatively rigid thoracic spine meets the mobile lumbar spine, and it is where imaging should look first when the clinical story fits.
A hip fracture after a fall from standing height late Report immediately
Why: The senile pattern: cortical-predominant loss at a femoral neck that is 30:70 trabecular to cortical. Lifetime hip fracture risk for women aged 50 and over is 17.5%, and 75% of hip fractures occur in women. A fracture from a fall that should not have broken anything is by definition a fragility fracture.
A distal radius (wrist) fracture in an older adult Hold & notify
Why: The third classic fragility site, appearing in the fracture-risk tables and in the treatment criteria — a proximal humerus, pelvis or distal forearm fracture in a person with low bone mass is itself an indication to treat. It often comes earlier than hip fracture and is therefore the warning that gets ignored.
Impaired gait, poor balance and reduced strength Hold & notify
Why: Gait, balance, strength and mobility "should be assessed at each clinical encounter to assess the likelihood of an impending fall and subsequent fracture," because sarcopenia runs alongside bone loss — 3% to 5% of muscle mass lost per decade from the fourth decade, worsening after 50. Bone that is fragile only fractures when something knocks it over, so fall risk is half the disease.
New dull aching pain in the thigh or groin in a patient on long-term bisphosphonate therapy Report immediately
Why: The prodrome of an atypical femoral fracture, which usually appears after more than 7 years of treatment: "initial symptoms are dull aching pain in the groin." The action is to discontinue immediately, because continuing therapy risks a contralateral fracture. This is the symptom patients must be taught to report before it becomes a completed fracture.
Flu-like aches, fever, myalgia, arthralgia and headache 1 to 3 days after a first zoledronic acid infusion Expected
Why: The acute phase reaction, with up to 30% risk with the first infusion. It resolves with acetaminophen or an NSAID. Teaching it before the infusion is what stops a patient believing they have caught an infection and refusing the next dose.
Signs of an underlying secondary cause — hormone excess or deficiency, malabsorption, or malnutrition Hold & notify
Why: Examination is directed at nail changes, hair loss, muscle wasting and altered menstruation, plus signs of hyperthyroidism, Cushing syndrome or hypogonadism. In a man, a secondary cause is more likely than not — secondary osteoporosis accounts for 50% to 80% of male cases against 30% of female cases.

Diagnostics

Test In this disorder Normal
Dual-energy x-ray absorptiometry (DXA) Radiation "is comparable to standard background radiation." The hip has the strongest correlation with fracture risk; the spine "demonstrates less variability and can detect earlier responses to treatment" but is "prone to interference from surrounding vasculature, calcification, and osteophytes," so expect a falsely high spine reading in an arthritic older adult. Per 1 SD decrease at the femoral neck, hip fracture risk rises 2.6-fold; per 1 SD at the lumbar spine, vertebral fracture risk rises 2.3-fold Measures bone mineral density in g/cm² at two routine sites — the lumbar spine (L1–L4) and the hip (femoral neck, greater trochanter, Ward’s area, intertrochanteric region and total hip) —
T-score versus Z-score — which patient gets which Using the wrong one misclassifies the patient. A Z-score of −2.0 or lower is below the expected range for that age and should prompt assessment for secondary causes — the single most useful lab signal that something other than aging is at work T-score compares the patient with a young-adult reference population matched for gender and race; Z-score compares with age-matched controls T-scores for postmenopausal women and men over 50. Z-scores for premenopausal women, men under 50, and children
WHO T-score categories Two reframes the number alone hides. First, more total fractures occur in the osteopenia range (−1.0 to −2.5) than below −2.5, simply because far more people sit there. Second, osteoporosis may also be diagnosed with a T-score between −1.0 and −2.5 when risk-assessment tools demonstrate increased fracture risk — and "regardless of the improvement in the T-score with treatment, the diagnosis of osteoporosis persists" ≥ −1.0 normal · between −1.0 and −2.5 osteopenia · ≤ −2.5 osteoporosis · ≤ −2.5 plus a fragility fracture = severe (established) osteoporosis WHO, as reported by StatPearls —
Screening — who and when Those thresholds belong to the Bone Health and Osteoporosis Foundation 2022 Clinician’s Guide — including the recommendation for men, which is BHOF’s, not the USPSTF’s — the USPSTF issues an I statement for men, meaning insufficient evidence to assess the balance of benefits and harms, which is not the same as a recommendation against screening. The USPSTF 2025 update (as reported by StatPearls) adds a Grade B recommendation to screen females younger than 65 with one or more risk factors — weight < 127 lbs, BMI < 21 kg/m², parental hip fracture, current tobacco use, or discontinuing estrogen. Repeat DXA no more often than every 1 to 2 years Women aged ≥ 65 and men aged ≥ 70 regardless of risk factors; postmenopausal women and men aged 50–69 based on risk profile; and any adult who fractures at age 50 or older BHOF 2022 Clinician’s Guide; USPSTF 2025 as reported by StatPearls —
FRAX 10-year fracture risk Inputs are age, sex, height, weight, prior fracture, parental hip fracture, tobacco, corticosteroids, rheumatoid arthritis, alcohol, secondary osteoporosis and femoral neck BMD. Know what it misses: it fails to include falls, certain medications linked to low BMD, or diabetes, and does not quantify corticosteroid dose, alcohol or cigarette use, or their duration. A faller with a reassuring FRAX is still a faller Treatment thresholds: 10-year hip fracture risk ≥ 3%, or 10-year major osteoporosis-related fracture risk ≥ 20%, in a patient with low bone mass BHOF 2022 Clinician’s Guide —
Baseline and secondary-cause laboratory workup Targeted additions by context: TSH for hyperthyroidism, intact PTH for hyperparathyroidism, serum protein electrophoresis with kappa/lambda light chains for myeloma, tissue transglutaminase IgA for celiac disease, 24-hour urinary free cortisol for Cushing syndrome, and gonadal hormones for hypogonadism. Vitamin D and calcium must be measured and corrected before an antiresorptive is started, because of hypocalcemia risk CBC; comprehensive metabolic panel including calcium, phosphate, total protein, albumin, alkaline phosphatase, liver enzymes, creatinine and electrolytes; 25-hydroxyvitamin D; and 24-hour urine calcium, sodium and creatinine excretion AACE, as reported by StatPearls —
Vertebral fracture assessment Because a third of vertebral fractures are found radiographically rather than clinically, imaging is how the silent ones are caught. For a symptomatic suspected fracture, start with AP and lateral spinal radiographs; MRI distinguishes acute from chronic fractures and identifies malignancy by abnormal marrow signal in pedicles or posterior elements and soft-tissue mass-like extension Obtain in a patient with a T-score ≤ −1.0 plus at least one of — female age ≥ 70, height loss ≥ 4 cm, prior vertebral fracture, or corticosteroid ≥ 5 mg prednisone daily for ≥ 3 months ISCD, as reported by StatPearls —
DXA sources of error a nurse can prevent Structural change from osteophytes, calcification or an existing fracture "potentially cause an artefactual component of BMD," and demographic-entry errors change the reference population. Practical rule: remove metal before the scan, and read a high spine score in an arthritic patient with suspicion Artifacts that alter the reported BMD: bra components, surgical clips, navel rings and vascular prostheses — plus positioning error from "excessive internal or external rotation of the proximal femur" —

Complications

Warning: Fragility fracture — and the cascade it starts Report immediately
37 million fragility fractures occur annually worldwide in people over 55; in the US, 1.9 million a year, projected to reach 3.2 million by 2040. Hip lifetime risk for women over 50 is 17.5%, vertebral 16.0%.
The first fracture is the heralding cue for the second: prior fracture roughly doubles future risk with the highest hazard in the first 2 years, and an existing vertebral fracture multiplies it five-fold. A 65-year-old with one vertebral fracture has a 1 in 4 chance of another within 5 years, halved to 1 in 8 by treatment. A hip or vertebral fracture is itself an indication to treat, regardless of the DXA T-score.
Warning: Mortality after fracture
For a 50-year-old White woman, the 2.8% lifetime risk of dying from a hip fracture equals her lifetime breast cancer death risk, and is four times her endometrial cancer risk.
European data from 2010 recorded 43,000 deaths after fracture — 50% from hip, 28% vertebral, 22% other in women. This comparison is the one that changes how patients hear the diagnosis: osteoporosis is not a cosmetic problem about posture, and a hip fracture is not a broken bone that simply heals.
Caution: Osteonecrosis of the jaw and atypical femoral fracture Hold & notify
Two rare but serious antiresorptive complications. Jaw osteonecrosis in osteoporosis treatment runs 1 in 10,000 to 1 in 100,000; atypical femoral fracture runs 3.2 to 50 cases per 100,000 person-years and is "usually not seen within the first five years of bisphosphonate treatment, with most cases reported with more than seven years."
Both are preventable or catchable. A dental check comes before the first dose — a detailed dental history before a bisphosphonate, and a baseline dental evaluation before denosumab; if invasive dental work is planned, initiation is delayed a few months, and an established user of more than 4 years stops the drug two months before the procedure. For atypical fracture, the prodrome is teachable: new dull aching pain in the groin or thigh — discontinue immediately, because continuing risks a contralateral fracture.
Warning: Rebound vertebral fractures after stopping denosumab Hold & notify
Stopping denosumab without a bridging drug causes "rapid loss of bone and rebound fractures (particularly vertebral)" — a risk related to treatment duration and more common in those with prior vertebral fractures.
The sourced rule is unambiguous: "Treatment interruption is not suggested. Denosumab should not be stopped without ensuing antiresorptive treatment (eg, bisphosphonate) to control a rebound in bone turnover and increased fracture risk." The nursing consequence is that a missed or delayed 6-month injection is not an adherence footnote — it is a fracture risk, and discontinuation must be planned with a transition to alendronate or zoledronic acid.
Caution: The treatment gap — non-adherence and missed diagnosis
Up to 30% never start a prescribed medication, about 50% discontinue bisphosphonates within a year, and up to 70% do not continue past a year. In one survey, 27% took a drug holiday or stopped — 47% of them without medical recommendation.
The companion failure is diagnostic: 35% of patients are unaware osteoporosis caused their fracture, nearly 50% blamed it on "clumsiness," and over 50% do not know one fracture predicts the next. Because the disease is silent, feeling well is misread as evidence the drug is unnecessary. Adherence counselling here is not administrative — it is the intervention that keeps the cascade from running.

Medications for this condition

Why each class is prescribed here — every card links to its full pharmacology page.

Bisphosphonates First-line
Musculoskeletal · alendronate

The default drug for osteoporosis — "the most commonly used therapeutic agents prescribed," and the first-line choice for anyone not at very high risk, with intravenous dosing when oral is contraindicated and denosumab as the alternative when bisphosphonates cannot be used, such as in renal failure. They bind hydroxyapatite at remodeling sites and shut down the osteoclast: nitrogen-containing agents inhibit farnesyl pyrophosphate synthase so the osteoclast detaches from bone, while non-nitrogen agents form a nonfunctional ATP analogue that triggers osteoclast apoptosis. The administration rules exist because oral absorption is under 3% even fasting — take it first thing in the morning, on an empty stomach, with a full glass of plain water, and stay upright for at least 30 minutes (30 to 60 per the osteoporosis chapter) before food or any other medication. Three disorder-specific safety points: correct vitamin D and calcium before the first dose, because hypocalcemia is the risk; obtain a dental examination first, because of osteonecrosis of the jaw; and know the renal floor — risedronate and ibandronate are not used below a GFR of 30 mL/min, alendronate and zoledronic acid below 35. Not every agent covers every fracture: alendronate, risedronate and zoledronate reduce vertebral, hip and nonvertebral fractures, but ibandronate reduces vertebral fractures only. Concomitant NSAIDs raise the gastrointestinal risk, and gastrointestinal effects are the commonest reason patients stop.
Electrolyte & Fluid Replacement High-alert
Renal

Calcium here is nutritional adequacy, not a treatment for osteoporosis — it is the substrate every antiresorptive and anabolic agent needs, and the deficiency that makes those drugs dangerous. The Bone Health and Osteoporosis Foundation 2022 targets are banded by age and sex: 1,000 mg/day for men aged 50–70, and 1,200 mg/day for women aged 51 and over and men aged 71 and over, with an upper limit of 2,000–2,500 mg/day. Food first is the sourced rule: "Increasing dietary calcium is the first-line approach, but calcium supplements should be used when an adequate dietary intake cannot be achieved" — and the gap is real, since average US intake is only 600 to 800 mg/day. On the cardiovascular question, the newest and highest-tier source settles it toward safety: BHOF 2022 reports that "a large systematic review and meta-analysis including RCTs and cohort studies found no evidence that calcium with or without vitamin D increased cardiovascular disease," with the VITAL study finding no adverse effects. Name the controversy if a patient raises it; do not tell them supplements cause heart attacks. The genuine caution is hypocalcemia before an antiresorptive — calcium and 25-hydroxyvitamin D are measured and corrected before the first bisphosphonate or denosumab dose.

Beyond medications

  • Exercise — the BHOF 2022 prescription is specific, not "stay active." A multicomponent program is recommended, including "progressive resistance training, balance training, back extensor strengthening, core stabilizers, cardiovascular conditioning, and impact or ground-reaction forces," with weight-bearing activities named as walking, jogging, tai chi, stair climbing, dancing and tennis. The dose is 30 minutes, 5 days per week (or 75 minutes twice weekly). Two facts about timing matter for expectation-setting: skeletal adaptation takes a minimum of about 8 months, and the benefit is lost if activity stops.
  • Fall prevention — the other half of the disease. The sourced modifiable list: "muscle strength and balance can be improved through targeted exercise; visual impairment can be addressed; severe vitamin D deficiency can be corrected; fall hazards in the home and work environment can be remediated." Multicomponent physical activity produced 22% lower risk of falls and 26% lower risk of injurious falls in meta-analysis, and tai chi specifically protects against falls. Devices where indicated: walkers or rollers for impaired mobility, and hip protectors for recurrent fall risk.
  • Vitamin D — always with its owner attached. The Institute of Medicine / National Academies intakes, reported inside BHOF 2022, are 600 units daily until age 70 and 800 units/day at 71 and over — this is where the familiar "600 to 800 IU" comes from. BHOF’s own recommendation is 800 to 1,000 units/day for adults aged 50 and over, with an upper limit of 4,000 units/day. AACE suggests 1,000 to 2,000 IU daily, higher in obesity or malabsorption. Never state an unowned number — the fetched guidance ranges from 400 to 2,000 IU depending on who is speaking. What everyone agrees on is the target: serum 25-hydroxyvitamin D at or above 30 ng/mL (BHOF adds an upper bound of 50 ng/mL). Also sourced: probiotics, magnesium, vitamin K1 and phytoestrogens are not recommended, excessive vitamin A is detrimental, and caffeine is limited to under 1 to 2 servings daily.
  • Denosumab — plain text, no class page. A fully human monoclonal antibody against RANKL, given as 60 mg subcutaneously every 6 months with no duration limit, reducing vertebral, hip and nonvertebral fractures, and usable in renal disease where bisphosphonates are not. Before each dose: check vitamin D, secure dental clearance, and correct pre-existing hypocalcemia — hypocalcemia can be "severe, even fatal," with the risk higher below a creatinine clearance of 30 mL/min. Patients need 1,000 mg calcium and 400 IU vitamin D daily. The rule that must never be omitted: it cannot simply be stopped. Discontinuation without a bridging bisphosphonate causes rapid bone loss and rebound vertebral fractures.
  • Anabolic agents — plain text, and the sequencing rule that ties them together. Teriparatide (PTH 1-34), 20 μg subcutaneously daily by pen, requires refrigeration; it reduces vertebral and nonvertebral fractures but has no demonstrated hip fracture reduction, and its osteosarcoma boxed warning was removed in November 2020. Abaloparatide, 80 μg daily, needs no refrigeration, is limited to 2 years total, and also has no demonstrated hip reduction. Romosozumab, an anti-sclerostin antibody acting as both antiresorptive and anabolic, is given as 210 mg monthly for up to 1 year, is approved in the US for females only, and is the only anabolic agent shown to reduce vertebral, hip AND nonvertebral fractures — carrying a current boxed warning for stroke and myocardial infarction, not to be started within a year of a myocardial infarction or stroke (FDA label). Every anabolic must be followed by an antiresorptive, or the gains are lost. In very-high-risk patients — a fracture within 12 months, a fracture on therapy, multiple fractures, T-score ≤ −3.0, high fall risk, or FRAX above 30% major or 4.5% hip — the anabolic goes first.
  • Raloxifene and hormone therapy — plain text, with narrow niches. Raloxifene 60 mg daily reduces vertebral fractures only, is also approved to prevent invasive breast cancer in high-risk women, and loses its skeletal benefit within 1 to 2 years of stopping; adverse effects include hot flashes, leg cramps, DVT and fatal stroke. Hormone therapy reduces vertebral, hip and nonvertebral fractures but needs 5 to 7 years for significant reduction, and its risk-benefit is favourable only under age 60 or within 10 years of menopause; progestin is added in anyone with a uterus, at the lowest dose for the shortest time. On stopping estrogen, BMD falls about 6% in the first year and returns to never-treated levels by 2 years. Combination therapy is not routinely recommended.
  • Managing the vertebral compression fracture itself. The sourced plan is "adequate analgesia, physical therapy, and in many cases, spinal bracing," with bracing for 4 to 12 weeks, discontinued when pain resolves and radiographic healing occurs — and early mobilization is emphasized alongside physical therapy. Vertebral augmentation is genuinely contested and is not standard care: vertebroplasty stabilizes without restoring height while balloon kyphoplasty partially restores height with less cement leakage and reportedly improves function faster than conservative care, but AACE "advises against either a kyphoplasty or vertebroplasty, citing unclear benefits and concern for increased risk of adjacent vertebral fractures," and the European Society would consider it only after 2 to 3 weeks of persistent pain despite analgesia. Risks include cement leak, persistent pain, infection, paralysis, pulmonary embolism and adjacent fractures.

Nursing considerations

The RN-specific layer — each action paired with the reason it matters.

Assessment & monitoring
Measure height at every encounter and act on a loss of 1.5 inches or more by requesting vertebral imaging.
Why: A height loss of 1.5 inches or more "is an indication to obtain vertebral imaging," and about a third of vertebral fractures are found radiographically rather than clinically. This is the one bedside measurement that detects a fracture the patient never felt.
Assess gait, balance and strength to predict fall risk, and survey the home environment for fall hazards.
Why: Fragile bone only breaks when something knocks the patient over, and sarcopenia runs alongside bone loss. Multicomponent physical activity produced 22% lower risk of falls and 26% lower risk of injurious falls — fall prevention sits beside drug therapy, not behind it.
Perform an oral examination as a baseline before any bisphosphonate or denosumab is started, and ask about planned dental work.
Why: Dental assessment comes first — "a detailed dental history before initiating bisphosphonates," and a baseline dental evaluation before denosumab — because of osteonecrosis of the jaw. Planned invasive dental work changes the plan: initiation is delayed a few months, and an established user of more than 4 years stops the drug two months beforehand.
Check that 25-hydroxyvitamin D, serum calcium and renal function are drawn and corrected before the first antiresorptive dose — not after.
Why: All patients "must have their vitamin D levels measured and treated before starting therapy due to the risk of hypocalcemia." With denosumab, hypocalcemia can be "severe, even fatal," and the risk is higher below a creatinine clearance of 30 mL/min. Renal function also sets which bisphosphonate is usable at all.
On follow-up, track BMD 1 to 2 years after initiation then every 2 years, and annually check height, weight, serum calcium, 25-hydroxyvitamin D and back pain.
Why: The disease is silent, so scheduled monitoring is the only feedback loop available. A new back pain report at an annual check is how the next vertebral fracture gets caught early rather than after the height has gone.
In any man with osteoporosis, and in anyone with a Z-score of −2.0 or lower, escalate for a secondary-cause workup.
Why: Secondary causes account for 50% to 80% of male cases against 30% of female cases — in a man, a secondary cause is more likely than not. A Z-score at or below −2.0 is "below the expected range for that age" and is the signal that something beyond aging is at work.
Interventions & safety
Give oral bisphosphonates first thing in the morning, on an empty stomach, with a full glass of plain water, and keep the patient upright for at least 30 minutes with nothing else by mouth.
Why: Oral absorption is under 3% even fasting, so anything in the stomach wastes the dose — and the upright rule prevents esophageal injury. The word plain matters: coffee, juice and mineral water all interfere. Do not give it to a patient who cannot sit or stand upright for 30 minutes; that is a stated contraindication.
Screen for the bisphosphonate contraindications before the first dose: hypocalcemia, esophageal disorders, GFR below 30 to 35 mL/min, malabsorptive states, and inability to remain upright.
Why: Achalasia, stricture, varices, Barrett’s esophagus and scleroderma all raise esophageal injury risk; celiac disease, Crohn’s and prior gastric bypass defeat an already marginal absorption. Risedronate and ibandronate stop at a GFR of 30; alendronate and zoledronic acid at 35.
Treat a missed or delayed denosumab injection as a clinical problem, not a scheduling one, and never let it be stopped without a bridging bisphosphonate.
Why: "Denosumab should not be stopped without ensuing antiresorptive treatment… to control a rebound in bone turnover and increased fracture risk." Discontinuation causes rapid bone loss and rebound vertebral fractures, particularly in patients who have already had one.
Warn the patient about the acute phase reaction before a first zoledronic acid infusion, and have acetaminophen available.
Why: Flu-like symptoms, fever, myalgia, arthralgia and headache occur within 1 to 3 days in up to 30% of first infusions and resolve with acetaminophen or an NSAID. Told in advance it is an expected reaction; discovered afterwards it looks like an infection and costs the next dose.
After a vertebral compression fracture, support analgesia, physical therapy, brace compliance and early mobilization — and do not impose an improvised movement restriction.
Why: The sourced management is "adequate analgesia, physical therapy, and in many cases, spinal bracing," with bracing for 4 to 12 weeks and early mobilization emphasized. Immobility costs bone, muscle and independence in a patient who is already losing all three.
Review the medication list for bone-losing drugs and flag them for the prescriber — glucocorticoids, proton pump inhibitors, SSRIs, antiepileptics, aromatase inhibitors, androgen deprivation therapy, heparin, thiazolidinediones, depot medroxyprogesterone.
Why: These are modifiable by review, and glucocorticoids in particular have a defined threshold: fracture risk is assessed at ≥ 2.5 mg prednisone equivalent for ≥ 3 months (American College of Rheumatology), while treatment in a postmenopausal woman is recommended at ≥ 7.5 mg prednisolone daily for ≥ 3 months (IOF/ECTS). The 3-month duration is agreed across all three sources.
Patient teaching
Teach explicitly that this fracture was caused by osteoporosis and predicts the next one — and give the number: 1 in 4 chance of another vertebral fracture within 5 years, reduced to 1 in 8 with treatment.
Why: 35% of patients do not know osteoporosis caused their fracture, nearly 50% blamed "clumsiness," and over 50% do not know that one fracture increases the risk of the next. Naming it converts an accident into a treatable diagnosis, which is what changes adherence.
Teach the atypical femoral fracture prodrome by name: new dull aching pain in the groin or thigh must be reported, not walked off.
Why: It usually appears after more than 7 years of bisphosphonate therapy, and the action is to discontinue immediately because continuing risks a contralateral fracture. Reported early it is a prodrome; ignored it is a completed femoral fracture.
Teach that feeling fine is not evidence the medication is unnecessary, and address drug holidays directly.
Why: Osteoporosis is a "silent" disease, and adherence collapses accordingly: up to 30% never start, about 50% stop within a year, and 47% of those who took a drug holiday did so without medical recommendation. A holiday is a reassessment after 5 years of oral or 3 years of intravenous bisphosphonate only in patients no longer at high risk — not an automatic stop.
Teach calcium food first, with the target banded by age and sex: 1,000 mg/day for men 50–70, 1,200 mg/day for women 51 and over and men 71 and over.
Why: "Increasing dietary calcium is the first-line approach, but calcium supplements should be used when an adequate dietary intake cannot be achieved" — and average US intake is only 600 to 800 mg/day, so most patients have a real gap to close. The upper limit is 2,000 to 2,500 mg/day.
Prescribe exercise as a multicomponent program — progressive resistance, balance, back extensor strengthening, core stabilizers, cardiovascular conditioning and impact — at 30 minutes, 5 days a week, and set the expectation that it takes about 8 months to show skeletal benefit.
Why: "Stay active" is too vague to follow. The specific components are named in the guideline, and both the delay before benefit and the fact that benefits are lost if activity stops are what keep a patient going through the months when nothing seems to be happening.
Address smoking cessation and alcohol moderation as bone interventions, not general health advice.
Why: Smokers carry a 30% increased fracture risk independent of BMD, and cessation "can lead to an increase in BMD and reduce fracture risk." More than 3 units of alcohol daily brings a 38% increase in major osteoporotic and 68% increase in hip fractures; AACE advises postmenopausal women to limit intake to no more than 2 units daily.

How a real nurse thinks

The clinical-judgment loop, worked for a typical presentation — reasoning, not reference.

  1. 1
    Recognize cues

    The cues assemble into one diagnosis. Acute back pain after minimal trauma, sharply worse on movement and standing and relieved by lying still, is the hallmark presentation of a vertebral compression fracture. The tenderness sits at T12–L1, within the thoracolumbar junction (T12 to L2), where 60% to 75% of vertebral compression fractures occur. The 5.1 cm (about 2 inch) height loss is well past the 1.5-inch threshold that is "an indication to obtain vertebral imaging," and the kyphosis is accumulated collapse made visible. The exposure is in the chart in plain sight: prednisone 10 mg daily for 14 months, with no calcium, no vitamin D, no bisphosphonate and no DXA. The reassuring cues also matter — no night pain, no multi-site pain, no weight loss, no cancer history, and no neurological deficit. And the most important cue is one she gave you herself: she believes this is normal aging.

  2. 2
    Analyze cues

    Two questions have to be answered in order. First, is this osteoporosis or something worse? The sourced red flags for a neoplastic cause — "nocturnal pain, pain at multiple skeletal sites, unexplained weight loss, or a known history of cancer," with multiple myeloma the particular concern — are all absent, which makes an osteoporotic fracture much more likely, but does not remove myeloma from the workup. Second, what does this fracture mean? It means the diagnosis is already made: a fragility fracture of the spine is an indication to treat regardless of the DXA T-score. Her steroid exposure crosses every threshold in the literature — ≥ 2.5 mg prednisone for ≥ 3 months triggers fracture-risk assessment per the American College of Rheumatology, and at 10 mg daily she is well past the ≥ 7.5 mg for ≥ 3 months at which IOF/ECTS recommends treating a postmenopausal woman. She is also "very high risk" by AACE criteria on the strength of a fracture within the last 12 months.

  3. 3
    Prioritize

    Imaging and pain control come first, because she cannot be assessed or mobilized while she is in 7/10 pain on movement, and because an acute fracture has to be distinguished from an old one. Second is the workup that has to happen before any drug is given — 25-hydroxyvitamin D, calcium, renal function, and a dental examination, because starting an antiresorptive into unrecognized hypocalcemia or untreated dental disease is how the treatment causes harm. Third is the diagnosis conversation, which is not optional filler: over half of patients in her position do not know that one fracture predicts the next, and she has already told you she thinks this is aging. Fourth is the DXA, which will guide the choice of agent and provide a baseline — but note that it does not gate the decision to treat. That decision is already made by the fracture.

  4. 4
    Generate solutions

    Anticipate AP and lateral spinal radiographs first, with MRI to distinguish an acute fracture from an old one and to exclude malignancy by marrow signal and soft-tissue extension. Anticipate analgesia, physical therapy, and spinal bracing for 4 to 12 weeks with early mobilization — not bed rest. Anticipate baseline 25-hydroxyvitamin D, calcium, renal function, CBC and metabolic panel, with serum protein electrophoresis and light chains in the secondary workup, plus TSH and intact PTH. Arrange the dental examination. Expect treatment to start: alendronate, teriparatide and denosumab are all approved for corticosteroid-induced osteoporosis, and her very-high-risk status argues for an anabolic first, followed by an antiresorptive. Start calcium at 1,200 mg/day for a woman over 51 and vitamin D per the prescriber’s chosen guideline, attributing the number.

  5. 5
    Take action

    Document the height loss with both measurements and the dates, because that is the objective finding that justifies imaging. Escalate with an SBAR: "72-year-old woman, prednisone 10 mg daily for 14 months, no bone protection and no DXA. Four days of acute T12–L1 back pain after minimal trauma, worse on movement. Height loss of 5.1 cm over 6 years with visible kyphosis, no neurological deficit, and none of the malignancy red flags. I am concerned about a glucocorticoid-related vertebral compression fracture. Requesting spinal imaging, analgesia, and baseline vitamin D, calcium and renal function — and she needs a dental exam before any antiresorptive." Three traps to avoid. Waiting for the DXA before treating — a vertebral fracture is an indication to treat regardless of T-score. Telling her not to bend or twist — no fetched guidance supports a flexion restriction, and the sourced management explicitly emphasizes early mobilization with bracing and physical therapy. And letting her leave believing this was clumsiness.

  6. 6
    Evaluate

    Success over the next weeks: pain controlled enough to mobilize, brace in use and being weaned as pain resolves and radiographic healing appears, physical therapy underway, calcium and vitamin D corrected, and bone-protective therapy started with the dental clearance done. The steroid itself gets revisited with the prescriber, since it is the ongoing driver. Over months: a multicomponent exercise program at 30 minutes five days a week, home fall hazards remediated, and a DXA as the baseline for monitoring at 1 to 2 years. The re-escalation triggers are set in advance: new leg weakness, numbness or bowel or bladder change means cord compromise; new dull groin or thigh pain on a long-term bisphosphonate means a possible atypical femoral fracture; and any new focal back pain means imaging again, because her risk of a second fracture is highest in the next two years.

Scenario — you’re the nurse

Work each question before revealing the answer. Rationales explain the wrong options too.

Outpatient clinic, urgent same-day appointment · 1115

A 72-year-old woman with polymyalgia rheumatica has been on prednisone 10 mg daily for the past 14 months. She reports four days of mid-back pain that began after she reached down to lift a bag of groceries from the car boot. The pain is sharp, much worse when she stands up or turns in bed, and eased by lying still. She has never had a DXA scan. She tells you she is "just getting old" and that her daughter noticed she seems shorter.

1115 vitals — HR 84 · BP 138/78 · RR 16 · T 36.8 °C · pain 7/10 on movement, 2/10 at rest
Assessment — focal tenderness over the T12–L1 spinous processes; visible thoracic kyphosis; no leg weakness, no saddle anesthesia, bowel and bladder continent
Height — 157.5 cm today · 162.6 cm recorded 6 years ago (loss of 5.1 cm, about 2 inches)
Chart — prednisone 10 mg daily × 14 months · no calcium or vitamin D supplement · no bisphosphonate · no DXA on file · no dental visit in 3 years
Patient report — no night pain, no weight loss, no cancer history; she says the pain is "only when I move"
Q1 Select all that apply
Which findings require follow-up? Select all that apply.
  1. A. Height loss of 5.1 cm over 6 years with visible thoracic kyphosis
  2. B. Acute T12–L1 back pain after lifting a bag of groceries
  3. C. Prednisone 10 mg daily for 14 months with no calcium, vitamin D or bisphosphonate
  4. D. No dental visit in 3 years
  5. E. Temperature 36.8 °C
Reveal answer & rationale
Answer: A, B, C, D
Height loss well past the 1.5-inch threshold with kyphosis (A) is "an indication to obtain vertebral imaging" and signals accumulated vertebral collapse. Acute focal back pain after minimal trauma (B) is the hallmark of a vertebral compression fracture, and T12–L1 sits within the thoracolumbar junction (T12 to L2), where 60% to 75% of them occur. Fourteen months of prednisone with no bone protection (C) crosses every sourced threshold — assessment at ≥ 2.5 mg for ≥ 3 months, treatment in a postmenopausal woman at ≥ 7.5 mg for ≥ 3 months. The dental history (D) matters because dental assessment is part of the pre-treatment workup for a bisphosphonate or denosumab, so it is a follow-up item that will delay therapy if left. A normal temperature (E) is reassuring against infection and requires no action.
Q2 Multiple choice
Imaging confirms an acute T12 compression fracture. The patient has never had a DXA scan. The nurse should understand that:
  1. A. Treatment cannot begin until a DXA confirms a T-score of −2.5 or lower
  2. B. A fragility fracture of the spine is an indication to treat regardless of the DXA T-score
  3. C. Treatment is deferred because she is on prednisone and steroids must be stopped first
  4. D. A DXA is unnecessary now that a fracture has occurred
Reveal answer & rationale
Answer: B
Treatment is indicated for a "fracture of the hip or vertebra regardless of BMD" (B) — the fracture has already demonstrated the bone fragility that the T-score is a proxy for. Waiting for the scan (A) delays therapy in a patient whose risk of a second fracture is highest in the next two years. Stopping the steroid first (C) is not the rule; prednisone is often clinically necessary, which is exactly why alendronate, teriparatide and denosumab are approved for corticosteroid-induced osteoporosis. And the DXA is still worth doing (D) — it guides agent selection and gives the baseline for monitoring at 1 to 2 years — it simply does not gate the decision to treat.
Q3 Put in order
Put the nurse’s priorities in order:
  1. A. Arrange the dental examination and baseline vitamin D, calcium and renal function before any antiresorptive is given
  2. B. Escalate for spinal imaging and analgesia
  3. C. Teach that the fracture was caused by osteoporosis and predicts another
  4. D. Arrange the DXA scan and multicomponent exercise referral
Reveal answer & rationale
Correct order: B → A → C → D
Imaging and analgesia come first (B): an acute fracture must be distinguished from an old one and from malignancy, and the patient cannot be mobilized at 7/10 pain on movement. The pre-treatment workup follows (A), because vitamin D levels must be "measured and treated before starting therapy due to the risk of hypocalcemia" and dental assessment comes before the first dose — both will otherwise delay the drug. Teaching (C) comes next and is genuinely therapeutic, since over half of patients do not know one fracture predicts the next and this patient believes she is simply aging. The DXA and exercise referral (D) matter for monitoring and long-term risk but neither changes today’s management.
Q4 Multiple choice
The patient is started on an oral bisphosphonate. Which statement by the patient indicates correct understanding?
  1. A. "I will take it with my breakfast so it does not upset my stomach."
  2. B. "I will take it first thing in the morning with a full glass of plain water and stay sitting up for at least 30 minutes before I eat anything."
  3. C. "I will take it at bedtime with a glass of milk for the extra calcium."
  4. D. "I will take it with my morning coffee and then lie back down for a while."
Reveal answer & rationale
Answer: B
Oral absorption is under 3% even fasting, so the drug must be the first thing taken, on an empty stomach, with a full glass of plain water — and the patient stays upright for at least 30 minutes before food or any other medication, which prevents esophageal injury (B). Taking it with breakfast (A) or with milk (C) destroys the already marginal absorption, and milk’s calcium specifically interferes. Coffee (D) is not plain water, and lying down afterwards is the exact action the upright rule exists to prevent — inability to remain upright for 30 minutes is a stated contraindication to the drug.
Q5 Multiple choice
Eight years later, still on alendronate, the patient reports several weeks of new dull aching pain in her right groin. The nurse should recognize this as:
  1. A. Expected osteoarthritis of the hip that can be managed with analgesia
  2. B. A possible atypical femoral fracture — report it, because the drug may need to be stopped immediately
  3. C. Referred pain from her old T12 fracture
  4. D. An expected side effect of alendronate that resolves on its own
Reveal answer & rationale
Answer: B
"Initial symptoms are dull aching pain in the groin" is the sourced prodrome of an atypical femoral fracture, which is reported mostly after "more than seven years of bisphosphonate treatment" — she is now in her eighth year — and the action is to discontinue immediately, because the risk of a contralateral fracture rises if therapy continues (B). Treating it as arthritis (A) or as referred pain (C) allows a stress lesion to progress to a completed femoral fracture. Calling it self-limiting (D) confuses it with the acute phase reaction, which is a different phenomenon entirely: flu-like symptoms within 1 to 3 days of a first zoledronic acid infusion, not weeks of groin pain years into oral therapy.

Common questions

What causes osteoporosis?
Common causes and risk factors include advancing age — 85% of nursing home residents over 80 have osteoporosis, female sex and postmenopausal status — about 80% of the 10.3 million affected americans are women, including 21.2% of women over 50 worldwide, a prior fragility fracture — roughly a two-fold increase in future risk, and a five-fold increase if the prior fracture was vertebral, family history — nearly 20% report a positive family history, and maternal hip fracture raises offspring risk, low body weight — under 127 lbs or bmi under 21 kg/m² increases fracture risk and is a named screening trigger, and others.
What are the early signs of osteoporosis?
Early findings include Nothing at all — osteoporosis is a "silent" disease.
Which findings should a nurse report immediately in osteoporosis?
Report immediately: Back pain that is nocturnal, at multiple skeletal sites, or paired with unexplained weight loss or a cancer history, A hip fracture after a fall from standing height, New dull aching pain in the thigh or groin in a patient on long-term bisphosphonate therapy, Fragility fracture — and the cascade it starts. These signal deterioration that needs rapid intervention.
How much calcium and vitamin D does someone with osteoporosis need?
Calcium per the Bone Health and Osteoporosis Foundation 2022 guideline is banded by age and sex: 1,000 mg/day for men aged 50–70, and 1,200 mg/day for women aged 51 and over and men aged 71 and over, with an upper limit of 2,000–2,500 mg/day. Food comes first — "increasing dietary calcium is the first-line approach, but calcium supplements should be used when an adequate dietary intake cannot be achieved" — and most people have a gap to close, since average US intake is only 600 to 800 mg/day. Vitamin D has to be quoted with its owner, because the fetched guidance genuinely disagrees: the Institute of Medicine / National Academies figures reported inside BHOF are 600 units daily until age 70 and 800 units/day at 71 and over, while BHOF’s own recommendation is 800 to 1,000 units/day for adults 50 and over (upper limit 4,000). Everyone agrees on the target to aim at: serum 25-hydroxyvitamin D of 30 ng/mL or above.
Do bisphosphonates have to be stopped after 5 years?
No — what happens at 5 years is a reassessment, not an automatic stop. BHOF 2022 says to "reassess patient and BMD status for consideration of a drug holiday after 5 years of oral and 3 years of intravenous bisphosphonate in patients who are no longer at high risk of fracture (T-score ≥ −2.5, no new fractures)." A patient who remains at high risk continues. Note that denosumab has no equivalent stopping point and behaves in the opposite way: stopping it without a bridging bisphosphonate causes rapid bone loss and rebound vertebral fractures, so "denosumab should not be stopped without ensuing antiresorptive treatment." A missed 6-month injection is a fracture risk, not a scheduling problem.
Do all osteoporosis drugs prevent hip fractures?
No, and choosing the wrong one for a patient whose main risk is hip fracture is a real error. Alendronate, risedronate and zoledronate reduce vertebral, hip and nonvertebral fractures. Denosumab also reduces all three, and is usable in renal disease where bisphosphonates are not. But ibandronate reduces vertebral fractures only, as do raloxifene and calcitonin. Among the anabolic agents, teriparatide and abaloparatide have no demonstrated hip-fracture reduction — romosozumab is the only one shown to reduce vertebral, hip and nonvertebral fractures, and it carries a current boxed warning for stroke and myocardial infarction. A further rule ties the anabolics together: every one of them must be followed by an antiresorptive, or the gains are lost.

Sources

Reviewed by Hae Suk Lee, RN

Educational summary for nursing students. Scenarios are fictional teaching cases. Always verify against current guidelines and your institution's protocols before acting in practice. Not medical advice.

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