Osteoporosis and fragility-fracture prevention

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

Treat a low-energy fracture as a mechanical and biological diagnosis. Record the exact fall, whether pain preceded it, previous fractures, height loss, glucocorticoid dose, menopause or hypogonadism, smoking, alcohol, nutrition, falls, medicines and family hip fracture. Establish baseline residence, walking aids, cognition and goals because these determine fixation, rehabilitation and discharge. Pain before the incident or an atypical radiograph should prompt a pathological-fracture differential rather than automatic attribution to osteoporosis.

Examine the injured region before focusing on long-term risk. Use trauma ABCDE when appropriate, expose the limb or spine, assess skin and deformity and document pulses, capillary refill, motor and sensory function. Immobilise a painful unstable limb and restrict loading until imaging defines safety. For possible hip fracture, use prompt analgesia including trained nerve block where available. Search for additional injuries and pressure risk in a frail patient who cannot reposition independently.

Obtain site-appropriate radiographs in orthogonal planes. If hip fracture remains clinically suspected after adequate films, NICE recommends MRI, or CT when MRI is unavailable within 24 hours or contraindicated. CT defines complex articular or peri-implant morphology, while MRI detects occult trabecular fracture and marrow disease. Vertebral-fracture assessment with DXA or lateral spine radiography identifies compression deformity; MRI is reserved for acute level, malignancy, infection or neurological questions.

Fracture pattern and bone quality shape surgery. Aim for stable reduction, load-sharing constructs and fixation that tolerates the patient's realistic rehabilitation. Arthroplasty can bypass weak femoral-head fixation in defined displaced intracapsular hip fractures. Long working lengths, multiple fixation points, cement augmentation or intramedullary load sharing may help selected osteoporotic patterns, but implant choice remains fracture- and patient-specific. Discuss ceilings of care without assuming that chronological age alone predicts benefit.

Once acute physiology is stable, start a secondary-prevention bundle. Calculate FRAX where useful, arrange DXA if it will refine rather than obstruct a decision, and request FBC, renal and liver profiles, adjusted calcium, phosphate, alkaline phosphatase and vitamin D; add thyroid, PTH, coeliac, testosterone or myeloma tests when indicated. Review falls, vision, footwear, blood pressure, cognition and home environment. A fracture liaison service should own tracking, treatment initiation and handover.

NOGG advises treatment without delay after a fragility fracture because risk clusters immediately after the event. Oral bisphosphonate suits a person able to follow fasting upright administration with adequate renal function and no major oesophageal problem. Intravenous zoledronic acid avoids weekly adherence and is a key option after hip fracture once calcium, vitamin D, renal function and acute clinical status are suitable. Explain the first-infusion flu-like reaction and plan renal and mineral checks.

Denosumab is useful when indicated but requires an exit strategy before the first injection. Give 60 mg subcutaneously every six months and ensure appointments are not casually deferred. If it must stop, specialist-planned antiresorption covers the rebound period. Teriparatide, abaloparatide or romosozumab may be selected for very-high-risk adults under current commissioning criteria, followed without avoidable gap by an antiresorptive. Romosozumab needs cardiovascular-risk assessment.

Rehabilitation is part of fracture prevention. Provide enough analgesia for breathing, transfers and gait practice; minimise sedatives; correct reversible delirium and nutrition problems; prescribe resistance and balance work; and fit aids that the patient can use. Calcium should preferably come from diet, with supplements and vitamin D targeted to deficiency or inadequate intake. Review treatment persistence and new fractures, but do not impose an automatic bisphosphonate holiday on someone whose risk remains high.

Key points

A fragility fracture follows force no greater than a fall from standing height and is a treatment trigger, not a reason to postpone prevention until DXA.
First-line orthopaedic assessment addresses the current fracture: mechanism, pre-injury function, pain, skin, distal neurovascular status, imaging in two planes and safe loading instructions.
Use FRAX for ten-year probability and add femoral-neck DXA when the result will alter treatment; a recent hip or vertebral fracture already establishes high risk.
Look actively for silent vertebral fractures when there is height loss, kyphosis, glucocorticoid exposure or suspicious spinal pain because they markedly change future risk.
Start secondary prevention promptly through a fracture liaison service while fracture care continues; avoid leaving the decision to an unspecified future primary-care review.
Oral alendronic acid or risedronate and intravenous zoledronic acid are usual first-line antiresorptive options; post-hip-fracture zoledronate is especially useful when oral adherence is doubtful.
Very-high-risk features such as a recent vertebral fracture, multiple vertebral fractures or extremely low BMD warrant specialist consideration of anabolic-first treatment followed by antiresorptive consolidation.
Never delay or stop denosumab without a documented next dose or sequential antiresorptive plan because rebound turnover can cause multiple vertebral fractures.

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

Ageing and menopause

Oestrogen loss accelerates resorption, while ageing reduces osteoblast function, calcium absorption, muscle power and balance; trabecular-rich vertebrae and the proximal femur become especially vulnerable.

Glucocorticoid exposure

Systemic corticosteroids rapidly impair formation, increase resorption and weaken muscle, so fracture risk rises early and can be substantial before bone-density values enter the osteoporotic range.

Secondary skeletal disease

Hyperthyroidism, hyperparathyroidism, hypogonadism, malabsorption, chronic liver or kidney disease, inflammatory illness, myeloma and several medicines can reduce strength or alter mineralisation.

Falls and frailty

Sarcopenia, impaired vision, postural hypotension, sedating medicines, unsafe footwear and environmental hazards determine whether weakened bone is exposed to a fracture-producing load.

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

1
Remodelling imbalance
When osteoclastic resorption repeatedly exceeds osteoblastic replacement, trabeculae perforate and cortex becomes porous, reducing structural redundancy as well as measured mineral quantity.
2
Microdamage accumulation
Ordinary loading creates microscopic cracks; impaired repair permits coalescence, so a standing-height fall or routine twist can exceed the remaining mechanical reserve.
3
Vertebral load failure
Trabecular loss allows anterior wedging or endplate collapse, which may be painless yet alters sagittal balance and concentrates load on adjacent vertebrae.
4
Imminent refracture period
Risk of another fracture is highest soon after an index event because skeletal weakness, falls drivers and loss of mobility remain active simultaneously.
5
Healing environment
Osteoporosis changes fixation purchase and construct mechanics more than basic biological union, requiring attention to reduction, load sharing, implant choice and rehabilitation safety.

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

Sentinel low-energy fracture

A hip, clinical vertebral, distal-radius or proximal-humeral fracture after a standing-height fall identifies skeletal fragility and predicts another event.

Occult hip fracture

Persistent groin pain, inability to bear weight or pain on axial loading despite normal radiographs requires urgent cross-sectional imaging.

Silent vertebral collapse

Height loss, kyphosis, reduced rib-pelvis distance or an incidental wedge deformity can reveal previous fracture without a remembered painful episode.

Very-high-risk pattern

Recent vertebral fracture, multiple vertebral fractures, extremely low BMD or fracture during treatment supports urgent specialist anabolic assessment.

Fixation-risk phenotype

Thin cortices, comminution, poor purchase, sarcopenia and inability to restrict loading increase construct failure risk and influence operative strategy.

Atypical femoral warning

New thigh or groin ache with lateral cortical thickening during prolonged antiresorption precedes some complete transverse femoral fractures.

Red flags requiring action

A painful deformed limb, inability to bear weight after trivial trauma or focal bony tenderness in an older adult may be a fracture even when bruising is slight.
A shortened externally rotated leg after a fall is a hip fracture until imaging proves otherwise; provide analgesia and follow the urgent hip-fracture pathway.
Sudden spinal pain with weakness, sensory level, saddle numbness or sphincter change requires immediate immobilisation decisions and emergency MRI assessment.
Multiple fractures, lytic change, hypercalcaemia, weight loss, anaemia or pain unrelated to movement suggests malignancy or myeloma rather than uncomplicated primary osteoporosis.
Atypical subtrochanteric or femoral-shaft pain during prolonged antiresorptive therapy requires bilateral femoral imaging and protected loading before a complete fracture occurs.
Jaw pain, exposed bone or an unhealed extraction site during potent antiresorptive treatment warrants dental or maxillofacial assessment without unplanned medicine cessation.

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
First-line fracture radiographsFirst stepFirst line
Why
Define location, displacement, articular involvement, bone texture and any destructive feature before loading or reduction decisions.
Interpretation and limitations
Obtain two planes and include adjacent joints where appropriate; a normal film cannot exclude occult hip, sacral or vertebral fracture.
02
MRI for radiographically occult hip fracture
Why
Identify marrow fracture when clinical suspicion persists despite adequate plain imaging.
Interpretation and limitations
MRI is the reference next study; use CT if MRI cannot be obtained within 24 hours or is contraindicated, and reconsider MRI if CT is negative but suspicion remains.
03
FRAX with selective femoral-neck DXA
Why
Estimate future major osteoporotic and hip-fracture probability and refine treatment thresholds.
Interpretation and limitations
Use BMD when it can change classification; do not let scanning postpone secondary prevention after a high-risk recent fracture.
04
Vertebral-fracture imaging
Why
Detect an unrecognised vertebral event in height loss, kyphosis, steroid exposure or compatible pain.
Interpretation and limitations
A vertebral fracture materially increases risk and may move the patient into a very-high-risk treatment pathway.
05
Secondary-cause and treatment-safety bloods
Why
Find mineral, endocrine, renal, hepatic, haematological or nutritional factors and establish medicine safety.
Interpretation and limitations
Interpret adjusted calcium, phosphate, ALP, vitamin D and renal function together; unexplained anaemia, hypercalcaemia or protein elevation warrants myeloma assessment.

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

Osteomalacia

Diffuse tenderness, proximal weakness, low phosphate or vitamin D and raised alkaline phosphatase suggest defective mineralisation rather than isolated loss of normally mineralised bone.

Myeloma or metastasis

Night pain, anaemia, renal dysfunction, hypercalcaemia, monoclonal protein or a destructive lesion requires oncological investigation and changes biopsy and fixation planning.

Paget disease

Focal expansion, cortical thickening and coarse trabeculae with disproportionate alkaline-phosphatase elevation indicate disordered high-turnover bone rather than generalised osteoporosis.

Atypical femoral fracture

Prodromal thigh pain and a transverse lateral-cortex lesion in the subtrochanteric or shaft region defines a stress-type complication needing a separate bilateral pathway.

Traumatic high-energy fracture

A substantial mechanism can fracture healthy bone; do not label every older-person injury fragility-related before reconstructing the force, pattern and possible pathological lesion.

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

01ImmediateProtect and define the fractureFirst stepA low-energy injury produces focal pain, deformity or loss of weight-bearing ability.

1Use ABCDE when indicated, provide analgesia and document skin, compartments and distal neurovascular findings.
2Immobilise the painful region and restrict loading until radiographs and orthopaedic review establish stability.
3EscalationEscalate open injury, threatened skin, hip fracture, neurological deficit and unstable vertebral features through emergency pathways.
4If hip-fracture suspicion persists after normal films, obtain MRI promptly or CT when MRI is unavailable within 24 hours or contraindicated.

02Early secondary preventionClose the post-fracture gapA fragility fracture is confirmed or strongly suspected.

1Refer to the fracture liaison service before discharge and name the clinician responsible for results and treatment.
2Assess FRAX, previous vertebral and hip fractures, falls, cognition, nutrition, medicines and secondary causes.
3Arrange DXA or vertebral imaging only where it refines care, without delaying risk-appropriate therapy.
4Provide written loading, rehabilitation, falls and medicine plans to the patient, GP and community team.

03PharmacologicalMatch potency and delivery to riskFracture probability or an index hip or vertebral fracture supports drug treatment.

1Correct hypocalcaemia and material vitamin-D deficiency and verify renal, dental and administration safety.
2First lineUse oral alendronic acid or risedronate, or intravenous zoledronic acid, as usual first-line choices according to risk and feasibility.
3Refer very-high-risk disease for anabolic-first consideration and record the antiresorptive treatment that must follow.
4Before denosumab, book six-monthly dosing and document a supervised discontinuation strategy.

04Long-termPrevent construct and patient failureThe fracture is healing and secondary-prevention treatment has begun.

1Progress loading according to fixation or fracture stability and measure transfers, gait, strength and confidence.
2Review adherence, adverse effects, falls and incident fractures rather than relying on repeat BMD alone.
3Reassess oral bisphosphonate near five years and intravenous treatment near three years, continuing when risk remains high.
4Investigate new thigh pain, jaw symptoms or fracture during therapy promptly and coordinate any medicine change.

Key medicines and prescribing safety3 treatments · regimens, roles and cautions

Reduces vertebral, non-vertebral and hip-fracture risk in suitable high-risk adults who can follow administration reliably.

Alendronic acid first-line oral antiresorptive

Use 70 mg orally once weekly, swallowed after an overnight fast with plain water while upright; wait at least 30 minutes before food, drink, other medicine or lying down.

Avoid in hypocalcaemia, important oesophageal emptying disease, inability to remain upright and severe renal impairment; correct vitamin-D deficiency and review dental risk.

Provides potent adherence-independent antiresorption and is a preferred option after hip fracture when clinically suitable.

Zoledronic acid after fragility fracture

Give 5 mg by intravenous infusion no faster than 15 minutes, usually once yearly, only after confirming hydration, creatinine clearance, corrected calcium and adequate vitamin-D and calcium provision.

Avoid when creatinine clearance is below the product threshold or hypocalcaemia persists; warn about acute-phase symptoms and rare jaw osteonecrosis or atypical femoral fracture.

Treats high fracture risk when selected through guideline and commissioning criteria, including some patients unsuitable for bisphosphonate.

Denosumab with mandatory continuity plan

Administer 60 mg subcutaneously every six months with adequate calcium and vitamin D; schedule each future dose and any sequential antiresorptive before treatment begins.

Correct hypocalcaemia, intensify calcium monitoring in advanced kidney disease, review infection and dental risk and never allow unplanned delay or cessation because rebound vertebral fractures can occur.

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

Hip fracture consequences

Pain, immobility, delirium, infection, thrombosis, loss of independence and excess mortality make prompt surgery and coordinated orthogeriatric care essential.

Vertebral deformity

Progressive height loss and kyphosis can cause chronic pain, restrictive breathing, abdominal crowding, impaired gaze and increased forward-fall risk.

Fixation failure

Poor screw purchase, comminution and inability to comply with restrictions can produce cut-out, varus collapse, peri-implant fracture or revision surgery.

Treatment-specific skeletal harm

Long antiresorptive exposure rarely causes atypical femoral fracture or jaw osteonecrosis, while unprotected denosumab withdrawal can precipitate clustered vertebral fractures.

Recurrent falls and fractures

Failure to address vision, strength, home hazards, medicines and postural blood pressure leaves the initiating mechanical exposure unchanged despite pharmacological treatment.

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

During acute care, repeat pain, skin, neurovascular and mobility assessment and check that loading instructions match the fracture and construct.
Track fracture-liaison referral, DXA or vertebral imaging, secondary-cause results and actual treatment initiation rather than recording advice alone.
Before and after parenteral therapy, monitor calcium, vitamin-D adequacy and renal function at intervals appropriate to the medicine and comorbidity.
Review falls, postural blood pressure, vision, footwear, sedating medicines, strength and home hazards after each new event.
Record denosumab injection dates and contact patients before a dose becomes late; escalation should precede any discontinuation.
At treatment review, consider interval fracture, adherence, glucocorticoids, age and updated probability before reducing or pausing therapy.

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

The fracture can diagnose risk

A recent hip or vertebral fragility fracture can justify treatment without waiting for a numerical DXA threshold.

Normal films do not clear the hip

An older patient unable to bear weight after a fall still needs occult-fracture imaging when initial radiographs are unrevealing.

Bone density is not bone strength

Architecture, turnover, microdamage, geometry and falls contribute to failure, so a T-score alone cannot explain every fracture.

Fixation must tolerate reality

A construct dependent on perfect non-weight-bearing may fail when frailty or cognition makes that restriction impossible.

Denosumab has no casual holiday

Its effect reverses rapidly, unlike retained bisphosphonate, making delayed injections and unsupported stopping actively hazardous.

Treat the imminent-risk window

The months after an index fracture offer the greatest opportunity to prevent another event and should not be lost to fragmented handovers.

11Common pitfallsFrequent interpretation and management errors.

01
Waiting for DXA before treating a recent high-risk hip or vertebral fragility fracture.
02
Assuming normal hip radiographs exclude fracture despite persistent inability to bear weight.
03
Writing advise GP to consider osteoporosis without an owned fracture-liaison handover and result plan.
04
Starting denosumab without booking the next injection and defining how treatment would later be stopped safely.
05
Ignoring focal thigh pain during prolonged antiresorptive exposure or failing to image the opposite femur.
06
Selecting fixation or loading instructions that the patient's cognition, strength or home support cannot realistically sustain.