Overview.
Osteoporosis is a systemic skeletal disorder characterised by reduced bone density and microarchitectural deterioration, leading to increased fracture risk. It affects approximately 10% of adults over 50 (200 million globally), with fracture rates doubling every decade after 50. The disease is almost entirely silent until a fracture occurs — making screening with DXA and blood markers essential. Bone loss accelerates dramatically in women during the 5-7 years surrounding menopause.
Bone is continuously remodelled — osteoclasts resorb old bone while osteoblasts form new bone. In osteoporosis, resorption exceeds formation, resulting in net bone loss. This imbalance is driven by oestrogen decline (menopause), aging, vitamin D/calcium deficiency, and secondary causes (medications, endocrine disorders). Blood markers track both the underlying causes and the rate of bone turnover.
Prevalence: ~10% of adults over 50 worldwide (~200 million). 1 in 2 women and 1 in 4 men over 50 will have an osteoporotic fracture. Hip fractures carry 20-30% one-year mortality in the elderly. Vertebral fractures are the most common but frequently undiagnosed (only 1/3 come to clinical attention).
Symptoms.
Early warnings
- Height loss >2 cm (vertebral compression fractures)
- Low-trauma fracture (fracture from fall from standing height or less)
- Kyphosis (increasing curvature of upper back)
- Vitamin D deficiency on blood work
- Low BMI (<20) or significant weight loss
- Corticosteroid prescription (bone protection should start immediately)
Classic symptoms
- COMPLETELY SILENT until fracture occurs — this is the defining feature
- Vertebral fractures: acute back pain, height loss, kyphosis (often found incidentally on imaging)
- Hip fractures: acute pain after fall, inability to bear weight
- Wrist fractures (Colles' fracture): often the first 'warning' fracture
- Chronic back pain from multiple vertebral fractures
- Reduced mobility and fear of falling
Progression
Peak bone mass is reached by age 25-30. After age 40, bone loss occurs at ~0.5-1% per year. In women, menopause accelerates loss to 2-3% per year for the first 5-7 years (total loss ~20% in that window). After this rapid phase, loss returns to ~1% per year. By age 70-80, cumulative loss may reach 30-40% of peak bone mass. Fracture risk roughly doubles with each standard deviation decrease in bone density.
Risk factors.
- Female sex (especially post-menopausal)
- Age >65 (women) or >70 (men)
- Low body weight (BMI <20)
- Family history of hip fracture
- Early menopause (<45 years) or premature ovarian insufficiency
- Corticosteroid use (≥5mg prednisolone for ≥3 months — most common secondary cause)
- Smoking
- Excessive alcohol (>3 units/day)
- Vitamin D deficiency
- Sedentary lifestyle / immobility
- Rheumatoid arthritis and other inflammatory conditions
- Malabsorption (celiac disease, IBD, gastric bypass)
- Hyperthyroidism, hyperparathyroidism
- Type 1 diabetes
- Chronic kidney disease
Lab interpretation.
Key biomarkers
- Vitamin D (25-OH) — Often low; essential for calcium absorption. Target ≥30 ng/mL, ideally 40-60 ng/mL for bone health. (primary)
- Calcium — Usually normal due to PTH compensation. Low calcium + low vitamin D = secondary hyperparathyroidism driving bone loss. (primary)
- ALP (Bone Alkaline Phosphatase) — Elevated in high bone turnover states. Confirms bone origin (vs liver) when GGT is normal. Elevated after fracture. (secondary)
- TSH — Screen for hyperthyroidism (accelerates bone loss) and hypothyroidism (treatment can cause bone loss if over-replaced) (secondary)
- PTH (Parathyroid Hormone) — Elevated PTH with low/normal calcium = secondary hyperparathyroidism from vitamin D deficiency (most common scenario). Elevated PTH with high calcium = primary hyperparathyroidism (requires parathyroid evaluation). Secondary hyperparathyroidism accelerates bone resorption. (primary)
- CTx (C-Terminal Telopeptide) — Bone resorption marker. Decreases 50-70% within 3-6 months of antiresorptive therapy. Best measured fasting, morning. Used to monitor treatment response. (secondary)
- P1NP (Procollagen Type 1 N-Terminal Propeptide) — Bone formation marker. Increases 50-100% within 1-3 months of anabolic therapy (teriparatide). IOF/IFCC recommended reference bone formation marker. (secondary)
- eGFR — CKD impairs vitamin D activation and calcium handling; renal osteodystrophy is distinct from primary osteoporosis (supportive)
Diagnostic criteria
- DXA scan T-score ≤-2.5 at lumbar spine, femoral neck, or total hip = osteoporosis
- T-score -1.0 to -2.5 = osteopenia (low bone mass, increased risk)
- Low-trauma fracture (especially vertebral or hip) = clinical osteoporosis regardless of DXA
- FRAX score ≥20% (10-year major osteoporotic fracture) or ≥3% (hip fracture) = treatment threshold (US guidelines)
- Blood tests diagnose CAUSES of osteoporosis, not osteoporosis itself — DXA is the diagnostic tool
Recommended panels
When & next steps.
When to test
- All women ≥65 years (DXA screening per USPSTF)
- All men ≥70 years
- Post-menopausal women <65 with risk factors (low BMI, smoking, family history, fracture history)
- Men 50-69 with risk factors
- Anyone starting or on long-term corticosteroids (≥3 months)
- Anyone with a low-trauma fracture at any age
- Conditions causing secondary osteoporosis (celiac, CKD, hyperthyroidism, hyperparathyroidism)
If suspected
- DXA scan (gold standard for diagnosis and monitoring)
- Blood work: vitamin D, calcium, phosphate, ALP, PTH, TSH, CBC, CMP
- Additional: tTG-IgA (celiac screen if unexplained osteoporosis), serum protein electrophoresis (myeloma if >60)
- Calculate FRAX score (10-year fracture probability)
- Vertebral fracture assessment (VFA) on DXA or lateral spine X-ray
If confirmed
- Vitamin D repletion to ≥30 ng/mL (ideally 40-60 ng/mL)
- Calcium: 1000-1200 mg/day total (diet + supplement if needed)
- Weight-bearing and resistance exercise (most effective non-pharmacological intervention)
- Fall prevention assessment (especially in elderly)
- Bisphosphonates: first-line pharmacotherapy (alendronate, risedronate, zoledronic acid)
- Denosumab: alternative for bisphosphonate-intolerant patients (note: rebound risk if stopped)
- Anabolic agents (teriparatide, romosozumab): for severe osteoporosis or fracture despite bisphosphonates
- Repeat DXA every 2 years to monitor treatment response
- HRT: effective for osteoporosis prevention in early menopause (risk-benefit discussion)
FAQs.
Can blood tests diagnose osteoporosis?
No — DXA scan diagnoses osteoporosis (T-score ≤-2.5). Blood tests identify the CAUSES of bone loss (vitamin D deficiency, hyperparathyroidism, celiac disease, hyperthyroidism) and monitor bone turnover rate. Both are needed — DXA tells you WHERE you are; blood tests tell you WHY and HOW FAST you're losing bone.
I'm only 45 — should I worry about osteoporosis?
Not yet for screening (DXA recommended at 65 for women, 70 for men unless risk factors exist). But NOW is when prevention matters most — the 5-7 years around menopause are when bone loss is fastest. Ensure vitamin D is 40-60 ng/mL, get adequate calcium, do weight-bearing and resistance exercise regularly, and avoid smoking.
Does weight-bearing exercise really help?
Yes — it's the most effective non-pharmacological intervention. Weight-bearing exercise (walking, jogging, stair climbing) and resistance training (weights) stimulate osteoblast activity and reduce fall risk. Swimming and cycling, while excellent for cardiovascular health, do not provide significant bone-loading stimulus.
I'm on corticosteroids — when should I worry about my bones?
Immediately. Corticosteroid-induced osteoporosis is the most common secondary cause. Bone loss begins within the first 3 months of treatment and is dose-dependent. Anyone on ≥5mg prednisolone (or equivalent) for ≥3 months should have DXA, vitamin D optimisation, and typically a bisphosphonate for bone protection.