Osteoporosis - prevention of fragility fractures
Exam Tips
- In UK exams, identify who to assess: all women >=65 and men >=75, plus younger adults with risk factors (for example prior fragility fracture, steroids, falls, low BMI).
- A normal or osteopenic DXA does not exclude clinically important fracture risk; combine BMD with FRAX/QFracture and prior fracture history.
- Always screen for secondary causes and red flags (weight loss, night pain, anaemia, hypercalcaemia features) before labelling as primary osteoporosis.
- For oral bisphosphonate counselling, examiners expect administration technique, renal limits, and warning about ONJ/atypical femoral fractures.
- Vertebral fractures are frequently silent; height loss and kyphosis in an older patient should trigger vertebral fracture assessment.
Definition
Osteoporosis is a systemic skeletal disorder in which reduced bone strength (low bone mineral density plus impaired bone microarchitecture) increases the risk of fragility fracture. It is usually clinically silent until a low-trauma fracture occurs, classically at the hip, vertebrae, or distal radius; vertebral fractures may also occur with minimal strain such as bending or lifting.
Pathophysiology
Bone remodelling becomes unbalanced, with osteoclast-mediated resorption outpacing osteoblast-mediated formation. Ageing reduces bone mass in both sexes, and post-menopausal oestrogen deficiency causes an accelerated phase of trabecular bone loss over several years; reduced testosterone in older men also contributes. Peak bone mass (genetics, nutrition including calcium/vitamin D, sex hormones, exercise) determines later reserve, while secondary disorders (for example hyperthyroidism, hyperparathyroidism, malabsorption, chronic inflammatory disease) further weaken bone quality and quantity. DXA quantifies BMD (WHO osteoporosis threshold T-score <= -2.5 at femoral neck), but fracture risk also depends on age, falls risk, prior fracture burden, and comorbidity, so many fragility fractures occur above the densitometric osteoporosis threshold.
Risk Factors
- Increasing age (risk rises independently of BMD)
- Female sex, especially post-menopause
- Previous fragility fracture (higher risk with multiple fractures; hip fracture history is high risk)
- Parental history of hip fracture
- Low BMI (<18.5 kg/m^2)
- Current or recent oral corticosteroid exposure (dose- and duration-related)
- Smoking
- Alcohol intake >=3 units/day (or >14 units/week in risk assessment)
- Falls risk (impaired vision, neuromuscular weakness/incoordination, cognitive impairment, sedative or alcohol use)
- Rheumatoid arthritis and other inflammatory arthropathies
- Secondary causes: hypogonadism/premature menopause, diabetes, hyperthyroidism, hyperparathyroidism, hyperprolactinaemia
- Malabsorption states (coeliac disease, IBD, chronic pancreatitis)
- Chronic kidney disease, chronic liver disease, COPD, immobility
- Medicines associated with increased fracture risk: SSRIs, PPIs, enzyme-inducing antiepileptics (for example carbamazepine), aromatase inhibitors, GnRH agonists, thiazolidinediones
Clinical Features
Symptoms
- Often none until fracture
- Acute back pain after vertebral compression fracture
- Hip, wrist, rib, pelvic, or proximal humerus pain after low-trauma fall
- Progressive loss of height
- Functional decline and reduced independence after fracture
Signs
- Thoracic kyphosis
- Documented height loss compared with previous measurements
- Local spinal tenderness in acute vertebral fracture
- Reduced mobility and frailty after fracture
- Deformity consistent with vertebral wedge compression
Investigations
Management
Lifestyle Modifications
- Weight-bearing and muscle-strengthening exercise; balance training to reduce falls
- Smoking cessation and alcohol reduction within UK recommended limits
- Falls prevention: vision review, medication review (especially sedatives), home hazard reduction
- Adequate calcium intake (about 700-1200 mg/day total) and vitamin D repletion; give supplements if intake/sunlight is insufficient
- Address reversible secondary causes (for example untreated thyrotoxicosis, hypogonadism, malabsorption)
Pharmacological Treatment
Oral bisphosphonates (first-line antiresorptive)
- Alendronic acid 70 mg orally once weekly
- Risedronate sodium 35 mg orally once weekly
- Ibandronic acid 150 mg orally once monthly
Take on an empty stomach with plain water; remain upright for at least 30 minutes (60 minutes for some ibandronate preparations). Avoid in significant oesophageal disease, inability to sit/stand upright, hypocalcaemia, and severe renal impairment (typically eGFR <35 mL/min for alendronate, <30 mL/min for risedronate/ibandronate). Counsel on rare osteonecrosis of the jaw and atypical femoral fractures with long-term use.
Intravenous bisphosphonate
- Zoledronic acid 5 mg IV once yearly
Useful when oral bisphosphonates are unsuitable or not tolerated. Check renal function and calcium/vitamin D before each dose; contraindicated in hypocalcaemia and severe renal impairment. Acute-phase flu-like reactions can occur after infusion.
RANKL inhibitor
- Denosumab 60 mg subcutaneously every 6 months
Option when bisphosphonates are unsuitable. Correct hypocalcaemia before starting and monitor calcium (higher risk in renal impairment). Do not stop abruptly without an alternative antiresorptive due to rebound vertebral fracture risk.
Anabolic/dual-action specialist therapies for very high risk severe osteoporosis
- Teriparatide 20 micrograms subcutaneously once daily (usually up to 24 months)
- Romosozumab 210 mg subcutaneously once monthly for 12 months
Initiated in specialist care after fracture risk stratification. After completion, follow with antiresorptive therapy to preserve gains. Romosozumab is avoided in patients with recent MI or stroke risk concerns.
Selective oestrogen receptor modulator / hormone options in selected patients
- Raloxifene 60 mg orally once daily
- Hormone replacement therapy (regimen individualised)
Raloxifene lowers vertebral fracture risk but not hip fracture risk and increases VTE risk. HRT may be considered in younger postmenopausal women with menopausal symptoms and low fracture risk profile after discussing breast cancer, VTE, and cardiovascular risk.
Calcium and vitamin D supplementation
- Colecalciferol 800 IU daily (typical maintenance dose)
- Combined calcium carbonate/cholecalciferol preparations (for example 1-2 tablets daily depending on product)
Use when dietary calcium or vitamin D status is inadequate; essential adjunct before and during potent antiresorptives to reduce hypocalcaemia risk.
Complications
- Hip fracture requiring admission, with substantial 1-year mortality and long-term disability risk
- Vertebral compression fractures (many clinically silent) causing chronic pain, height loss, kyphosis, reduced function
- Kyphosis-related respiratory compromise and gastrointestinal symptoms
- Forearm and other fragility fractures causing pain, loss of independence, and reduced quality of life
- Increased mortality in the year after major fragility fracture
Prognosis
Prognosis depends on baseline frailty, age, fracture history, and treatment adherence. Without intervention, fracture risk is recurrent and cumulative; with risk-factor modification plus appropriate anti-osteoporosis therapy, future fracture risk can be reduced substantially, though prior hip or vertebral fracture signals persistent high risk and need for long-term review.
Sources & References
🏥BMJ Best Practice(1)
💊BNF Drug References(7)
- Ascorbic acid[management.pharmacological]
- Erythromycin[management.pharmacological]
- Oseltamivir[management.pharmacological]
- Pizotifen[management.pharmacological]
- Raloxifene hydrochloride[management.pharmacological]
- Risedronate sodium[management.pharmacological]
- Undecenoic acid with zinc undecenoate[management.pharmacological]
✅NICE Guidelines(1)
📖Textbook References(4)
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1537)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1563)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1580, 1581)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1580, 1581)[context]