Fragility fracture and secondary prevention

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

Treat the fracture first and then treat the fracture risk. Low-energy hip, vertebral, wrist, humeral and pelvic fractures are sentinel events even when the person describes a definite trip. Record mechanism, all previous adult fractures, height loss, back pain, family hip fracture, menopause or hypogonadism, smoking, alcohol, falls, glucocorticoid dose and duration and medicines that affect bone or balance.

A fracture liaison service systematically identifies patients, verifies fracture, assesses falls and skeletal risk, starts or recommends treatment and confirms follow-through. This closes the common gap between orthopaedic care and long-term prevention. Assign named ownership for blood tests, dental issues, medicine administration, exercise and monitoring rather than issuing an unowned recommendation at discharge.

Estimate risk with FRAX or QFracture where appropriate. FRAX can be calculated without BMD and then recalculated with femoral-neck BMD when DXA will alter classification. Clinical judgement modifies calculated probability for dose-dependent glucocorticoids, multiple or recent fractures, very low BMD, falls and discordant lumbar disease. A score is not a reason to postpone treatment in a clearly high-risk recent-fracture presentation.

DXA is the reference clinical test for bone mineral density, usually at hip and lumbar spine, but it measures density rather than all bone strength. Interpret artefact from degenerative spinal disease, vertebral collapse or metal. Use vertebral fracture assessment or lateral radiographs when there is height loss, kyphosis, acute or chronic back pain, glucocorticoid exposure or high fracture probability because an occult vertebral fracture can change urgency and treatment choice.

Assess secondary causes before or alongside treatment. Common tests include FBC, renal function, calcium, phosphate, alkaline phosphatase, liver tests, thyroid function and vitamin D according to local pathway. Add CRP or ESR, serum electrophoresis and light chains, coeliac serology, parathyroid hormone, testosterone or other tests when history, examination or results suggest inflammation, myeloma, malabsorption, hyperparathyroidism or hypogonadism.

Oral bisphosphonates are cost-effective first-line options for many patients. Alendronate is commonly given as 70 mg once weekly: swallow it with plain water on rising after an overnight fast, keep the torso upright for the following 30 minutes, and take no other drink, food or tablets during that period. Check the current product instructions, ability to comply, oesophageal disease, swallowing, calcium, vitamin D and renal function. Risedronate is an alternative with its own label.

Intravenous zoledronate 5 mg once yearly avoids oral absorption and adherence problems and is useful after hip fracture once calcium, vitamin D, hydration and renal function are suitable. Check creatinine clearance using the relevant product method; severe renal impairment is a contraindication. Explain acute-phase symptoms, provide appropriate analgesia advice and monitor calcium risk in susceptible patients.

Denosumab 60 mg subcutaneously every six months can be used when indicated, including when renal function limits bisphosphonates, but hypocalcaemia risk rises in severe CKD and specialist coordination is needed. It is not a casual temporary treatment: do not omit, delay or stop an injection without a planned transition, commonly to a bisphosphonate, because rebound vertebral fractures can occur.

Very-high-risk patients—such as those with recent or multiple vertebral fractures, extremely low BMD or fracture despite therapy—need prompt specialist assessment for anabolic-first or other intensified treatment. Teriparatide is given as 20 micrograms subcutaneously daily for a finite licensed course in appropriate patients, then followed by antiresorptive therapy to preserve gain. Romosozumab selection requires cardiovascular-risk and licensing review.

Calcium and vitamin D enable safe therapy but are not complete secondary prevention. Aim for adequate dietary calcium and replace vitamin D deficiency; supplements are used when intake is insufficient. Address protein, weight, smoking and alcohol. Provide progressive strength and balance exercise, vision and foot care, postural and medicine review and trained home-hazard intervention.

Review adherence, administration, interval fractures, falls, height and new back or thigh pain. Reassess oral bisphosphonate treatment commonly after at least five years and IV bisphosphonate after at least three years, but continue longer in high-risk people and do not impose an automatic holiday. Denosumab does not have a drug-holiday model. Plan dental prevention without unnecessarily delaying urgent fracture treatment.

Key points

A fragility fracture usually follows force equivalent to a fall from standing height or less and is a clinical signal for prompt secondary prevention.
First-line after acute care is fracture-liaison or equivalent coordinated assessment of fracture site, prior fractures, falls, medicines, nutrition, secondary causes and future risk.
Do not delay treatment simply to obtain DXA when an older person with a recent fragility fracture is already at high or very high risk and treatment is indicated.
Use FRAX or QFracture within its validated population and interpret clinical modifiers; DXA refines risk when it will affect treatment or monitoring.
Vertebral fracture assessment or lateral spine imaging is indicated when height loss, kyphosis, back pain, glucocorticoids or risk suggests occult vertebral fracture.
First-line antiresorptive choices commonly include oral alendronate or risedronate, or intravenous zoledronate when oral administration is unsuitable, selected for renal, gastrointestinal and adherence factors.
Denosumab 60 mg subcutaneously every six months is effective in selected patients but must not be delayed or stopped without a planned alternative antiresorptive strategy.
Very-high-risk disease, especially vertebral fracture burden, may warrant specialist anabolic treatment such as teriparatide followed by antiresorptive therapy.
Correct hypocalcaemia and vitamin-D deficiency before potent antiresorptive treatment and ensure adequate calcium intake, preferably through diet.
Secondary prevention also requires progressive balance and strength exercise, vision and medication review, home intervention and recovery of mobility.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Primary osteoporosis

Ageing, menopause, low peak bone mass and genetic susceptibility reduce bone strength through loss of trabecular connectivity and cortical thinning.

Secondary osteoporosis

Glucocorticoids, hypogonadism, hyperthyroidism, hyperparathyroidism, malabsorption, inflammatory disease, organ failure and some medicines accelerate bone loss. The pattern and associated features guide targeted investigation and treatment.

Falls and mechanical exposure

Poor balance, weakness, posture hypotension, vision loss and environmental hazards determine whether reduced skeletal strength is challenged.

Imminent fracture state

A recent fragility fracture marks very high near-term risk because skeletal vulnerability, falls and functional decline persist together.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Remodelling imbalance
Osteoclast resorption exceeds osteoblast formation, reducing bone quantity and deteriorating microarchitecture. Fragile bone then fails under loads that previously caused no injury.
2
Glucocorticoid effects
Glucocorticoids suppress bone formation, impair calcium balance and cause muscle weakness, producing early fracture risk not fully captured by bone density.
3
Vertebral cascade
One vertebral fracture alters spinal mechanics and predicts further vertebral fractures, pain, kyphosis and respiratory restriction.
4
Post-fracture acceleration
Pain, fear and immobility reduce strength and vitamin-D exposure and increase falls during the period when refracture risk is highest.
5
Antiresorptive discontinuation
Denosumab withdrawal permits rapid rebound in bone turnover and vertebral fracture risk unless followed by an effective antiresorptive plan.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Hip fragility fractureRed flag

Groin pain, shortened externally rotated leg or inability to weight bear after low trauma requires urgent hip imaging.

Clinical vertebral fracture

New focal back pain, height loss or kyphosis after minor loading suggests vertebral compression.

Silent vertebral fracture

Progressive height loss or kyphosis can reveal unrecognised vertebral collapse on targeted imaging.

Very-high-risk pattern

Recent vertebral or hip fracture, multiple vertebral fractures or very low BMD may justify specialist anabolic-first assessment.

Atypical femoral warningRed flag

New persistent thigh or groin pain during long antiresorptive exposure can precede an incomplete femoral fracture.

Pathological fracture patternRed flag

Atypical site, lytic lesion, constitutional symptoms or biochemical abnormalities require malignancy or metabolic evaluation.

Red flags requiring action

Inability to weight bear or pain on hip rotation after a standing-height fall requires hip-fracture assessment even if the initial radiograph is normal.
New limb weakness, saddle change, sphincter dysfunction or progressive neurological signs with vertebral pain requires emergency spinal imaging.
Night pain, weight loss, hypercalcaemia, anaemia or a lytic lesion suggests malignancy or myeloma rather than uncomplicated osteoporosis.
Fever, recent bacteraemia or immunosuppression with vertebral pain raises discitis or vertebral osteomyelitis concern.
New thigh or groin pain during long-term antiresorptive treatment requires imaging for an incomplete atypical femoral fracture.
Dental infection, severe renal impairment, hypocalcaemia or an unplanned denosumab interruption requires treatment-specific specialist review.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Fracture confirmation and site imagingFirst step
Why
Define the acute injury and stability.
Interpretation and limitations
Use radiographs first and MRI or CT for clinically suspected occult hip or selected vertebral, pelvic or pathological fracture.
02
FRAX or QFracture
Why
Estimate future major fracture probability.
Interpretation and limitations
Interpret age, prior fracture, glucocorticoids, falls and other modifiers; use thresholds and clinical context rather than score alone.
03
DXA
Why
Measure reference bone mineral density when it informs care.
Interpretation and limitations
Use femoral-neck and lumbar values with artefact awareness; a fragility fracture can justify treatment even without an osteoporotic T-score.
04
Vertebral fracture assessment
Why
Detect clinically silent vertebral collapse.
Interpretation and limitations
Image when height loss, kyphosis, pain, glucocorticoids or risk indicates, because a vertebral fracture changes risk category.
05
Baseline bone blood tests
Why
Identify contraindications and common secondary causes.
Interpretation and limitations
Check renal function, calcium, phosphate, alkaline phosphatase, liver, FBC, thyroid and vitamin-D context, tailoring to the person.
06
Directed secondary-cause tests
Why
Investigate an atypical skeletal phenotype.
Interpretation and limitations
Use myeloma, coeliac, parathyroid, sex-hormone, inflammatory or other testing when clinical or biochemical clues support it.
07
Falls and functional assessment
Why
Reduce the mechanical trigger for refracture.
Interpretation and limitations
Assess gait, balance, strength, posture, cognition, vision, medicines, footwear, home hazards and recovery goals.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Malignancy or myeloma

Disproportionate pain, lytic or atypical lesions, anaemia, renal dysfunction and hypercalcaemia require directed investigation. Serum, urine and imaging tests are selected from the specific accompanying clues.

Osteomalacia

Osteomalacia can produce diffuse bone discomfort and girdle weakness; biochemical clues include inadequate vitamin D, hypophosphataemia and increased alkaline phosphatase.

Infection

Fever, inflammatory markers, bacteraemia risk and focal spinal pain raise osteomyelitis or septic disease. Prompt cultures and imaging are needed because delay can cause neurological harm.

Traumatic fracture in normal bone

A high-energy mechanism can fracture normal bone and does not itself establish osteoporosis. The force and fracture pattern should therefore be documented accurately.

Degenerative or muscular pain

Osteoarthritis and soft-tissue pain can mimic vertebral or pelvic fracture but require examination and imaging when acute focal symptoms persist.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01First-line post-fracture sequenceTreat promptly during the imminent-risk periodFirst stepFirst lineA low-trauma fracture is confirmed or strongly suspected.

1Complete acute fracture care and identify previous and occult vertebral fractures, falls and secondary-cause clues.
2Estimate risk and obtain DXA only when it will refine management without delaying indicated therapy.
3Start appropriate anti-osteoporosis treatment, exercise and falls intervention through fracture-liaison follow-up.

02Antiresorptive selectionMatch route to safety and adherenceBone resorption treatment is indicated for fracture prevention.

1Check calcium, vitamin D, renal, dental, gastrointestinal and administration factors and explain options.
2Use oral bisphosphonate when feasible or IV zoledronate or another licensed option when more appropriate.
3Monitor adherence and new symptoms and reassess duration by drug and residual risk rather than an automatic holiday.

03Very-high-risk routeConsider bone-forming treatment earlyRecent or multiple vertebral fractures, very low BMD or fracture despite therapy suggests very high risk.

1Refer promptly for specialist review and exclude secondary causes and treatment failure from non-adherence.
2Select licensed anabolic or intensified therapy using fracture, renal, cardiovascular and cancer context.
3Follow an anabolic course with antiresorptive treatment so gains are maintained.

04Denosumab continuity routePrevent rebound vertebral fractureDenosumab is planned, due or must be discontinued.

1Confirm calcium and vitamin-D safety and agree a reliable six-month administration system before initiation.
2Avoid unplanned delay and monitor hypocalcaemia risk, particularly in advanced CKD.
3AlternativeIf stopping, arrange specialist-timed alternative antiresorptive treatment rather than a treatment gap.

Key medicines and prescribing safety4 treatments · regimens, roles and cautions

Cost-effective first-line oral antiresorptive for many people at high fracture risk.

Alendronic acid

70 mg orally once weekly; take on rising after an overnight fast with plain water, remain upright and avoid food, drink and other medicines for at least 30 minutes.

Avoid with oesophageal emptying disorder, inability to remain upright, hypocalcaemia and severe renal impairment; review dysphagia, upper gastrointestinal symptoms and adherence.

First-line-equivalent parenteral bisphosphonate when oral treatment is unsuitable and useful after hip fracture.

Zoledronic acid

5 mg by intravenous infusion once yearly, with infusion duration and renal checks according to the product information.

Correct hypocalcaemia and vitamin-D deficiency, ensure hydration, check creatinine clearance and avoid severe renal impairment; acute-phase reaction can follow the first dose.

Licensed antiresorptive for selected patients at increased fracture risk, including when other options are unsuitable.

Denosumab

60 mg subcutaneously once every six months.

Correct hypocalcaemia, monitor high-risk CKD closely, maintain dental care and never stop or delay without an alternative antiresorptive plan.

Specialist anabolic option for selected very-high-risk osteoporosis, particularly severe vertebral disease.

Teriparatide

20 micrograms subcutaneously once daily for the licensed maximum treatment duration, followed by antiresorptive treatment.

Avoid in hypercalcaemia, skeletal malignancy or radiotherapy and other label exclusions; review renal, calcium and orthostatic effects.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Recurrent fracture

Risk is greatest soon after an index fracture, particularly for hip and vertebral events. This imminent-risk period makes prompt secondary prevention particularly valuable.

Pain and deformity

Vertebral collapse causes chronic pain, height loss, kyphosis, reduced pulmonary space and impaired balance. Multiple fractures may also impair sleep, appetite and safe transfers.

Loss of independence

Hip and pelvic fractures can cause permanent mobility and ADL decline and increased care needs. Recovery requires coordinated analgesia, rehabilitation, equipment and social support.

Treatment complications

Oesophagitis, renal injury, hypocalcaemia, osteonecrosis of the jaw and atypical femoral fracture require drug-specific prevention and surveillance.

Mortality and carer burden

Hip and multiple vertebral fractures increase mortality, institutionalisation and household support requirements. These outcomes make prevention and rehabilitation important beyond the radiographic diagnosis.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Confirm that fracture-liaison identification led to an assessment, treatment start and named long-term owner.
Record interval fractures, falls, height loss, new back pain and persistent thigh or groin pain.
Review oral administration technique and adherence or on-time injection and infusion delivery.
Monitor renal function, calcium and vitamin D at intervals appropriate to the selected treatment and comorbidity.
Reassess fracture risk and treatment duration by drug-specific guidance; do not create a denosumab gap.
Track strength, balance, mobility, home intervention and return to meaningful activity alongside BMD.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

The fracture is the risk test

A recent low-trauma fracture can establish high urgency even before DXA is available.

Spine fractures hide

Height loss and kyphosis may be the only evidence, yet finding one changes future risk markedly.

Falls and bone need parallel care

Strong bone treatment cannot prevent head injury, and exercise alone cannot correct severe skeletal fragility.

Route solves different problems

IV treatment may solve swallowing and adherence but adds renal, infusion and acute-phase considerations.

Denosumab has no casual exit

Its biological rebound makes the stopping plan part of the initiation decision.

Review does not mean stop

A duration checkpoint reassesses residual risk; high-risk people often continue or switch treatment.

11Common pitfallsFrequent interpretation and management errors.

01
Treating the acute fracture without initiating secondary prevention.
02
Waiting months for DXA before treating an obviously high-risk recent fracture.
03
Assuming a normal lumbar DXA excludes fragility when degenerative change inflates density.
04
Starting an oral bisphosphonate without checking swallowing, posture and administration feasibility.
05
Giving zoledronate without renal, calcium, vitamin-D and hydration assessment.
06
Starting denosumab without a reliable repeat-dose and discontinuation plan.
07
Using calcium and vitamin D as the only therapy for high fracture risk.
08
Calling all low-trauma fractures osteoporosis without considering malignancy, osteomalacia or infection clues.