Lucan · Conditions

Osteoporosis

Australian guidance: RACGP Osteoporosis Management Guidelines + ANZBMS

1. Definition and epidemiology

Osteoporosis is characterised by low bone mineral density (BMD) and microarchitectural deterioration of bone tissue, leading to decreased bone strength and increased fracture risk following minimal trauma such as a fall from standing height or less. In Australia, approximately 3% of men and 13% of women aged 50 to 69 years meet the World Health Organization (WHO) definition, rising to 13% of men and 43% of women over 70 years; by 2022, an estimated 6.2 million Australians aged over 50 years were projected to have osteoporosis or osteopenia, with total direct and indirect costs predicted to reach $3.84 billion. The residual lifetime risk of minimal trauma fracture is approximately 44% for women aged over 60 years and 25% for men in the same age group, placing fracture risk above that of some common cancers and comparable to that of diabetes.

2. Pathophysiology

Normal bone undergoes continuous remodelling through coordinated osteoclast resorption and osteoblast formation. In osteoporosis, osteoclast activity outpaces osteoblast activity, producing net loss of cortical and trabecular bone mass. In postmenopausal women, falling oestrogen reduces inhibition of receptor activator of nuclear factor kappa B ligand (RANKL), accelerating osteoclast differentiation and trabecular thinning, perforation, and loss of connectivity. In men, declining testosterone and oestrogen with ageing drives a slower but comparable imbalance. Secondary causes amplify this mechanism: glucocorticoids suppress osteoblast activity and upregulate RANKL; androgen deprivation therapy (ADT) for prostate cancer and aromatase inhibitor (AI) therapy for breast cancer both deplete sex steroid support to bone. The resulting skeleton is mechanically weaker particularly at vertebral bodies and the femoral neck, the sites of highest trabecular content and clinical fracture burden (Robbins Ch 26 Bones).

3. Clinical presentation and diagnostic criteria

Osteoporosis is a silent disease: skeletal deterioration proceeds without symptoms until a fracture occurs, making case finding rather than population screening the recommended AU strategy. Vertebral fractures may be asymptomatic or present with acute back pain and are often detected only radiographically. Progressive loss of vertebral height produces increasing thoracic kyphosis, loss of standing height, and chronic back pain. Hip and peripheral fractures typically follow falls and present with acute pain and functional loss; hip fracture carries approximately 20% one-year mortality in women. The WHO diagnostic criterion, used by the Australian Pharmaceutical Benefits Scheme (PBS) to determine medication eligibility, defines osteoporosis as a BMD T-score of minus 2.5 or below (2.5 or more standard deviations below the young adult mean), osteopenia as a T-score between minus 1.0 and minus 2.5, and normal as minus 1.0 or above. A presumptive clinical diagnosis can be made in any patient aged over 50 years who sustains a minimal trauma fracture, even without BMD confirmation.

4. Investigations and AU-specific cutoffs

The first step in any patient over 50 years with a minimal trauma fracture or one or more major risk factors is formal clinical risk factor assessment to guide BMD measurement. BMD measurement by dual energy X-ray absorptiometry (DXA) scanning should cover at least two skeletal sites, including the lumbar spine and proximal femur (recommendation 4, grade A). The Fracture Risk Assessment Tool (FRAX) is used to calculate 10-year absolute fracture risk. In the AU-specific context, case finding with FRAX is recommended for those aged over 50 with lifestyle and non-modifiable risk factors: if FRAX risk for major osteoporotic fracture (MOF) is 10% or above, refer for DXA; if less than 10%, DXA is not routinely indicated. After DXA, FRAX is recalculated using the BMD result; pharmacological treatment is indicated when the T-score is minus 2.5 or below, or when the T-score is between minus 1.5 and minus 2.5 AND the FRAX MOF risk is 20% or above or the FRAX hip fracture risk is 3% or above. Secondary investigations to exclude secondary causes include serum calcium, phosphate, alkaline phosphatase, 25-hydroxyvitamin D (25(OH)D), parathyroid hormone (PTH), full blood count, thyroid-stimulating hormone, liver function tests, serum protein electrophoresis, and renal function. Vitamin D deficiency is defined as 25(OH)D less than 50 nmol/L for the purposes of supplementation decisions in patients on osteoporosis therapy.

5. Management

Management integrates lifestyle modification, supplementation, falls prevention, and pharmacotherapy. All patients should implement falls prevention, weight-bearing and resistance exercise, and dietary and alcohol modification regardless of fracture risk. Calcium supplementation is recommended when dietary intake is below 1300 mg per day; vitamin D supplementation corrects serum 25(OH)D below 50 nmol/L in those on osteoporosis medications. Frail and institutionalised older people should receive calcium, vitamin D, and adequate protein as standard of care (recommendation 12, grade B). Exercise should include at least twice-weekly progressive resistance training, most-days weight-bearing impact exercise, and challenging balance training (recommendation 17, grade B). Patients with very high or imminent fracture risk (T-score minus 3.0 or below, recent fracture, or FRAX MOF risk 30% or higher) should be referred promptly to a bone specialist for osteoanabolic therapy as first-line (recommendation 6, grade C). Bisphosphonates are first-line for high fracture risk in women and men over 50 (recommendation 22, grade A women / C men); reconsider after 5 to 10 years if the patient responds well (recommendation 23). Denosumab is recommended for postmenopausal women at high fracture risk (grade A) and as a bisphosphonate alternative in men (grade B), but cessation requires transition to bisphosphonate for at least 12 months to prevent rebound vertebral fracture (recommendation 26, grade C). Romosozumab is first-line at very high fracture risk in women (grade A) and men (grade C). SERMs are an option where vertebral fracture risk dominates and other agents are not tolerated, particularly in younger postmenopausal women with a breast cancer history (recommendation 30, grade A). Teriparatide is indicated in those who fracture on antiresorptive therapy or are at very high fracture risk (recommendations 31 and 32, grades A and C).

6. Pharmacology and AU PBS notes

PBS-listed bisphosphonates: alendronate (Fosamax, 70 mg orally weekly), risedronate (Actonel, 35 mg weekly or 150 mg monthly), zoledronate (Aclasta, 5 mg intravenous yearly). Authority applies for prior minimal trauma fracture or T-score minus 2.5 or below. Denosumab (Prolia, 60 mg subcutaneous every 6 months) is PBS-listed for postmenopausal women at high fracture risk and as alternative in men; denosumab cessation mandates sequential bisphosphonate for at least 12 months. Romosozumab (Evenity, 210 mg subcutaneous monthly for 12 months) is PBS-listed for postmenopausal women at very high risk; as a sclerostin inhibitor with dual anabolic and antiresorptive action it is contraindicated within 12 months of myocardial infarction or stroke. Teriparatide (Forteo, 20 micrograms subcutaneous daily) is PBS-listed for up to 18 months at very high risk or after fracture on antiresorptive therapy. Raloxifene (60 mg orally daily) is PBS-listed where vertebral fracture risk predominates; it reduces vertebral but not hip fracture risk.

7. Complications and monitoring

Key complications include hip fracture (approximately 20% one-year mortality), vertebral fracture (height loss, kyphosis, chronic pain), medication-related osteonecrosis of the jaw (MRONJ), and atypical fracture of the femur (AFF) with prolonged bisphosphonate use. MRONJ risk should be assessed before commencing therapy; high-risk patients require dental review first. Invasive dental procedures in patients on denosumab should be timed just before the next 6-monthly injection when bone suppression is at its lowest (recommendation 45, grade C). Monitoring: clinical review at 3 to 6 months after initiating pharmacological therapy, then every 6 to 12 months for side effects and adherence (recommendation 34, grade C); DXA interval is individualised to fracture risk and treatment response; bone turnover markers such as procollagen type 1 amino-terminal propeptide (PINP) are confined to specialist practice (recommendation 35, grade D). Fracture risk should be reassessed regularly in those not receiving therapy but at elevated risk (recommendation 33, grade C). Men on continuous ADT require bone health review every 1 to 2 years (recommendation 43, grade C).

Written for Australian practice and grounded in the guidance named above. Study material only — not medical advice. Always check against current guidelines.