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OverviewAetiologyPathophysiologyClinical features and red flagsInvestigationsDifferential diagnosisManagementComplicationsMonitoring and follow-upSpecial situationsCommon pitfallsQuestionsSources
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Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.

Osteoporosis risk assessment and treatment

Endocrinology and metabolism · UK scope · Sources checked 27 Aug 2026 · Clinical review pending

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A recent fragility fracture signals imminent risk

Hip fracture, painful vertebral collapse or another low-trauma fracture needs analgesia, mobilisation planning and rapid fracture-liaison assessment. New leg weakness, saddle sensory change or bladder-bowel disturbance with vertebral collapse requires emergency spinal imaging and surgical assessment rather than routine osteoporosis review.

Action: Manage the acute fracture and falls injury first, check calcium, renal function and vitamin D safety, and involve a fracture liaison or specialist service promptly. Do not postpone bone protection for months while awaiting perfect lifestyle change; very-high-risk features may justify specialist anabolic-first treatment.

Overview

Estimate fragility-fracture risk, identify secondary causes and start timely bone protection with explicit duration, adherence and discontinuation planning.

Fracture probability integrates age, prior fracture, parental hip fracture, smoking, glucocorticoids, rheumatoid arthritis, secondary osteoporosis, alcohol and femoral-neck BMD when available. NOGG 2024 uses FRAX to place adults into low, intermediate, high or very high risk relative to age-dependent and upper assessment thresholds. Do not order DXA reflexively for every older person: a clear high-risk decision after hip or vertebral fracture should not be delayed by scanning, while an intermediate probability is refined with BMD. Vertebral fractures are often clinically silent; height loss, kyphosis, long-term glucocorticoids or acute back pain can justify vertebral fracture assessment or lateral imaging. Examine gait and falls risk, and test full blood count, renal and liver profile, calcium, phosphate, alkaline phosphatase, vitamin D and thyroid or other secondary causes according to phenotype.

Practice

Two practice questions

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Endocrinology and metabolismOriginal SBA

Planning denosumab discontinuation

A high-risk patient receiving denosumab wants to stop after several years and has no contraindication to intravenous bisphosphonate. What is the safest principle?

Choose one answer, then submit
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Sources and review status5 sources · checked 27 Aug 2026 · clinical review pending+
Sources

Sources and review status

National guidance is shown before implementation-dependent detail. Typical adult dose examples remain subject to patient factors, contraindications and the live BNF or specialist protocol. Source check completed 27 Aug 2026; clinical approval remains outstanding.

  • NOGG 2024 full guidelineUK risk stratification, treatment selection, duration and sequencing.
  • NOGG pharmacological optionsBisphosphonate, denosumab, anabolic and discontinuation recommendations.
  • NOGG management strategyReassessment, treatment review and long-term planning.
  • NICE TA464 bisphosphonatesCost-effective oral and intravenous bisphosphonate treatment.
  • NICE CG146 fracture risk assessmentClinical fracture risk assessment and appropriate BMD use.

Editorial contact: Doctor’s Passport editorial team. Source-check date is separate from clinical approval. Report a content problem · Content changes

Authoring stateComplete draftClinical stateAwaiting reviewJurisdictionUnited Kingdom
Treatment is a long strategy, not a one-off prescription. Oral bisphosphonates require correct fasting administration and the ability to remain upright; intravenous zoledronate helps when adherence or upper gastrointestinal disease is problematic but needs renal assessment and can cause an acute-phase reaction. Denosumab is not retained in bone, so its effect reverses rapidly when a six-monthly dose is missed; NOGG recommends an intravenous zoledronate transition around six months after the final injection, with specialist marker-guided follow-up where available. Anabolic agents such as teriparatide, abaloparatide or romosozumab are selected through current NICE commissioning and specialist evaluation for very-high-risk patients, and must be followed without delay by antiresorptive treatment. Reassess after the planned course rather than authorising endless repeat prescriptions. Dental health, thigh or groin pain, renal function, calcium-vitamin D sufficiency, falls and new fractures determine safety and efficacy.

Key points

  • Osteoporosis is a disorder of reduced bone strength and fragility fracture risk; many fractures occur above a DXA T-score of minus 2.5, so density is not the whole diagnosis.
  • Use FRAX without BMD initially for appropriate adults, then obtain DXA when the result will refine an intermediate decision or provide a useful baseline.
  • A prior or recent fragility fracture, multiple vertebral fractures, very low BMD or high-dose glucocorticoids can define high or very high risk requiring prompt treatment.
  • Look for secondary causes including glucocorticoids, hypogonadism, hyperthyroidism, hyperparathyroidism, coeliac disease, myeloma, CKD, malabsorption, alcohol and immobilisation.
  • Oral alendronate or risedronate and intravenous zoledronate are cost-effective first-line options for many high-risk adults; renal, oesophageal and adherence factors guide route.
  • Denosumab is effective but should not be delayed or stopped without a pre-arranged antiresorptive transition because rebound vertebral fractures can occur.
  • Very-high-risk patients, particularly with vertebral fractures, need specialist consideration of anabolic treatment followed immediately by antiresorptive consolidation.
  • Falls assessment, strength and balance work, smoking and alcohol advice, adequate calcium-protein-vitamin D and fracture liaison care remain necessary alongside medicines.

Aetiology

01

Age and sex-steroid loss

Ageing and reduced oestrogen or androgen accelerate bone loss and weaken microarchitecture, particularly after menopause or prolonged hypogonadism.

02

Glucocorticoid and endocrine disease

Long-term glucocorticoids, hyperthyroidism, hyperparathyroidism and other endocrine disorders alter bone formation, resorption or calcium physiology for as long as the driver persists.

03

Low loading or nutritional reserve

Immobility, low body mass, malnutrition, vitamin D deficiency, alcohol and smoking reduce skeletal strength or increase falls and fracture risk.

04

Previous fragility fracture

A prior low-trauma fracture identifies established skeletal vulnerability and predicts further fracture independently of a single bone-density result.

Pathophysiology

  1. 1
    Remodelling balance shifts

    Bone resorption exceeds formation through age, sex-steroid deficiency, glucocorticoid exposure or secondary disease as the process continues.

  2. 2
    Bone mass and architecture deteriorate

    Trabeculae thin and lose connectivity while cortical porosity increases, reducing the skeleton's ability to distribute ordinary mechanical loads without fracture.

  3. 3
    Fragility fracture occurs

    A fall from standing height or routine movement can exceed weakened bone strength, commonly affecting vertebra, hip, wrist or humerus.

  4. 4
    Fracture risk compounds

    Pain, kyphosis, immobility and falls after one fracture further reduce function and increase the likelihood of another.

Clinical features and red flags

Fragility fracture

A fracture after a fall from standing height or less, especially hip, vertebral, wrist or humerus, indicates impaired bone strength and predicts further fractures.

Silent vertebral fracture

Height loss, kyphosis, unexplained back pain or incidental vertebral deformity on chest or abdominal imaging may reveal high-risk disease despite no recalled trauma.

Very high risk

Recent or multiple vertebral fractures, very low BMD, high glucocorticoid exposure or exceptionally high FRAX probability supports urgent specialist assessment and possible anabolic-first therapy.

Secondary osteoporosis

Young age, disproportionate density loss, anaemia, diarrhoea, endocrine symptoms, renal disease or fractures despite treatment should prompt a cause search rather than automatic medicine switching.

Treatment complication

Thigh or groin pain may precede atypical femoral fracture; exposed jaw bone or poor healing needs dental assessment, although both complications remain rare relative to benefit in high-risk patients.

Investigations

  1. 01
    FRAX calculationFirst step
    Why
    Estimate ten-year major osteoporotic and hip fracture probabilities from validated clinical risk factors, initially without BMD when appropriate.
    Interpretation and limitations
    Compare with current NOGG thresholds to reassure, request DXA, treat or refer. Adjust clinical judgement for dose-dependent risks and recent or multiple fractures not fully captured.
  2. 02
    DXA of hip and spine
    Why
    Measure BMD to refine fracture probability, document osteoporosis and provide a repeatable baseline where it changes care.
    Interpretation and limitations
    Use the relevant T-score or Z-score context. Artefact from degenerative spine disease can falsely elevate BMD; fracture risk and treatment indication are not erased by a T-score above minus 2.5.
  3. 03
    Vertebral fracture assessment or lateral imaging
    Why
    Detect occult vertebral compression in people with height loss, kyphosis, glucocorticoids or suggestive pain.
    Interpretation and limitations
    One or more vertebral fragility fractures markedly increases risk and can move a patient towards specialist very-high-risk treatment.
  4. 04
    Bone and renal biochemical profile
    Why
    Confirm calcium and vitamin D safety and identify CKD, osteomalacia or parathyroid disease before treatment.
    Interpretation and limitations
    Correct hypocalcaemia and vitamin D deficiency before parenteral antiresorptive therapy. Marked ALP, calcium, phosphate or eGFR abnormality needs cause-specific evaluation.

Differential diagnosis

01

Osteomalacia

Defective mineralisation causes diffuse bone pain, proximal weakness and biochemical abnormalities, whereas osteoporosis has normally mineralised but quantitatively weakened bone.

02

Metastatic or myeloma bone disease

Night pain, anaemia, weight loss, renal impairment or focal destructive lesions require malignancy assessment rather than routine osteoporosis treatment.

03

Paget disease

Focal expanded bone, characteristic radiographs and raised turnover confined to affected sites indicate disordered remodelling rather than generalised osteoporosis.

04

Degenerative spinal disease

Mechanical back pain and osteophytes may coexist, while height loss or acute focal pain should prompt assessment for an occult vertebral fracture.

Management

01AssessStratify fracture probabilityFirst stepAge, risk factor, glucocorticoid exposure or low-trauma fracture raises concern for osteoporosis.+
  1. 1Record fracture timing and mechanism, parental history, smoking, alcohol, glucocorticoid dose, comorbidity, falls and secondary-cause clues.
  2. 2Calculate FRAX and apply current NOGG thresholds, obtaining DXA and vertebral imaging when they will refine the risk category or treatment choice.
  3. 3Treat recent fracture promptly and refer very-high-risk disease for specialist anabolic consideration rather than waiting for routine serial BMD.
02TreatChoose a deliverable regimenFracture probability or fragility-fracture history crosses the treatment threshold.+
  1. 1Correct calcium-vitamin D deficiency, assess kidney and dental status, explain expected fracture benefit and match route to oesophageal, adherence and preference factors.

Complications

01

Hip fracture

A low-trauma hip fracture causes major pain, surgery, immobility and loss of independence and carries substantial subsequent health risk.

02

Vertebral fracture

Often silent vertebral collapse causes height loss, kyphosis, chronic pain and impaired respiratory and physical function.

03

Fracture cascade

One fragility fracture predicts further events, particularly soon afterwards, unless skeletal and falls risks are addressed.

04

Treatment-discontinuation harm

Unplanned interruption of some antiresorptive therapies can rapidly restore high bone turnover and precipitate vertebral fractures.

Monitoring and follow-up

  • Review oral adherence and administration technique early, because a prescription does not establish absorption or persistence.
  • Use a robust six-month denosumab recall and escalation system and identify missed appointments before the therapeutic window closes.
  • Reassess fracture risk at the drug-specific treatment milestone and after any new fracture, major risk factor or long glucocorticoid change.
  • Repeat DXA on the same machine or comparable site when the result will change continuation, pause or escalation, not at arbitrary short intervals.
  • Ask about dental symptoms and thigh or groin pain, investigate suspected osteonecrosis or atypical fracture promptly, and keep absolute risk in perspective.
  • Track falls, strength, vision and postural symptoms, because a stable BMD does not show whether fall exposure has improved.

Special situations

Imminent risk is front-loaded

A recent fracture predicts another soon, so fracture liaison assessment and treatment should begin promptly rather than after slow elective investigation.

T-score is not the threshold

Age and clinical factors can create high absolute fracture probability with osteopenic BMD. FRAX and prior fracture keep these patients visible.

Denosumab has no holiday

Unlike bisphosphonate retained in bone, its antiresorptive effect reverses quickly. A late dose is a clinical safety incident, not a benign pause.

Sequence protects gains

Anabolic therapy builds new bone but its benefit dissipates without immediate antiresorptive consolidation. The follow-on drug belongs in the original plan.

FRAX is not response monitoring

The calculator helps reassess current probability but does not directly measure whether an individual medicine worked. Fractures, adherence and BMD trends supply that context.

Common pitfalls

  1. 01

    Reassuring a patient with a fragility fracture because the DXA T-score is above minus 2.5.

  2. 02

    Delaying bone protection after hip or vertebral fracture until an elective scan months later.

  3. 03

    Starting oral bisphosphonate without teaching fasting and upright administration or checking oesophageal contraindications.

  4. 04

    Allowing denosumab to lapse because it is mistakenly treated like a bisphosphonate holiday.

  5. 05

    Completing an anabolic course without arranging immediate antiresorptive consolidation.

  6. 06

    Treating BMD while ignoring falls, vision, sedating medicines and secondary causes.

  • 05
    Secondary-cause screen
    Why
    Investigate blood, endocrine, gastrointestinal or malignant drivers suggested by age and phenotype.
    Interpretation and limitations
    Select full blood count, inflammatory markers, thyroid, coeliac, testosterone, protein electrophoresis or PTH rather than applying a fixed exhaustive panel to everyone.
  • 06
    Falls and functional assessment
    Why
    Identify balance, strength, vision, postural blood pressure, footwear, environmental and medicine risks that bone drugs cannot correct.
    Interpretation and limitations
    A positive assessment warrants targeted exercise, medicine review and multidisciplinary intervention; fracture prevention needs both fewer falls and stronger bone.
    • 2
    AlternativeStart oral bisphosphonate or intravenous zoledronate for most high-risk adults, or a current NICE-approved alternative when these are unsuitable.
  • 3Document duration and review date at initiation, arrange adherence and adverse-effect checks, and address falls, exercise, smoking, alcohol and nutrition in parallel.
    • 03SequenceStop or switch without reboundDenosumab, anabolic therapy or a long bisphosphonate course is due to end or change.+
    1. 1Reassess current FRAX with BMD where useful, interval fractures, adherence, renal function and the ongoing risk that originally justified therapy.
    2. 2Never allow denosumab to lapse without specialist-planned antiresorptive cover; use NOGG timing and bone-turnover monitoring where available.
    3. 3Follow anabolic therapy immediately with alendronate, zoledronate or denosumab, and plan bisphosphonate pauses only for suitable lower-risk patients with future reassessment.
    Key medicines and prescribing safety4 treatments · regimens, roles and cautions+
    Suppresses osteoclast activity and reduces vertebral, non-vertebral and hip fracture risk in appropriately selected high-risk adults.

    Alendronic acid

    Use the licensed once-weekly osteoporosis regimen, taken after an overnight fast with plain water while upright, delaying food and other medicines for the product-specified interval.

    Avoid or seek specialist advice in significant oesophageal disease, inability to sit upright, hypocalcaemia or renal impairment beyond the product limit. Review jaw risk and persistent thigh or groin pain.

    Provides potent antiresorptive treatment when oral adherence or gastrointestinal administration is unsuitable and is a first-line option after hip fracture.

    Intravenous zoledronic acid

    Give the licensed osteoporosis infusion at the NOGG and local protocol interval after checking calcium, vitamin D, hydration and creatinine clearance; administer through a trained service.

    Acute-phase symptoms, hypocalcaemia and kidney injury occur. Avoid below the product renal threshold, review dental and atypical-femur risk, and do not confuse the osteoporosis regimen with oncology schedules.

    Inhibits RANK ligand and reduces vertebral, non-vertebral and hip fractures when an alternative antiresorptive is appropriate.

    Denosumab

    Administer the licensed 60 mg subcutaneous dose every six months through a reliable recall system after calcium and vitamin D safety checks.

    Hypocalcaemia risk rises in advanced CKD. Do not delay or stop without a planned bisphosphonate transition because rapid rebound bone turnover and multiple vertebral fractures can follow.

    Builds bone or has dual anabolic-antiresorptive effects in selected people at very high fracture risk, especially with vertebral disease.

    Anabolic osteoporosis therapy

    Use teriparatide, abaloparatide or romosozumab only for the NICE-approved duration and eligibility through a specialist bone service, followed immediately by antiresorptive therapy.

    Contraindications and commissioning differ by agent; romosozumab requires cardiovascular-risk review, and teriparatide is unsuitable in specified metabolic bone or malignancy contexts. Benefit is lost without consolidation.