Osteoporosis — Symptoms, Causes & Treatment | MyMedicPlus

Osteoporosis is a systemic skeletal disease characterised by low bone mineral density (BMD) and microarchitectural deterioration of bone tissue, causing increased bone fragility and susceptibility to fragility fractures — fractures occurring from low-energy trauma (fall from standing height or less) at sites not typically fractured by significant force. It is diagnosed by dual-energy X-ray absorptiometry (DEXA) T-score at or below -2.5 standard deviations below the mean peak bone mass of a young adult reference population at the lumbar spine or femoral neck. The T-score between -1 and -2.5 defines osteopenia (low bone mass, not yet osteoporosis). Osteoporosis affects approximately 200 million people worldwide — disproportionately post-menopausal women (1 in 3 women and 1 in 5 men over 50 will sustain an osteoporotic fracture during their lifetime). The condition causes 8.9 million fractures annually, including 1.6 million hip fractures, 1.7 million wrist fractures, and 1.4 million vertebral fractures. Despite its massive global disease burden, osteoporosis is markedly under-diagnosed — over 80% of patients presenting with their first fragility fracture have not previously been treated for osteoporosis (the 'treatment gap'). Hip fracture carries 20-30% one-year mortality and leaves 50% of survivors with permanent disability. The economic cost of osteoporotic fractures in Europe alone exceeds €37 billion annually. Bone is a dynamic tissue — continuously remodelled by osteoclasts (resorption) and osteoblasts (formation) in a balanced cycle that is disrupted in osteoporosis, with resorption exceeding formation.

Primary osteoporosis: postmenopausal osteoporosis (Type I) — oestrogen deficiency after the menopause removes oestrogen's inhibition of osteoclast-mediated bone resorption, accelerating trabecular (cancellous) bone loss at 2-3% per year for 5-10 years post-menopause; predominantly affects vertebral bodies and distal radius. Age-related osteoporosis (Type II — senile osteoporosis) — affects both sexes over 70 from declining osteoblast function, reduced intestinal calcium absorption, secondary hyperparathyroidism, and reduced vitamin D synthesis; predominantly hip and femoral neck (cortical bone). Secondary osteoporosis (up to 30% of postmenopausal and 50% of male osteoporosis): glucocorticoid-induced osteoporosis (GIO) — the most common secondary cause — oral prednisolone above 7.5mg/day suppresses osteoblast function and stimulates RANKL expression (accelerating osteoclast activity); bone loss is most rapid in the first 3-6 months; bisphosphonates must be co-prescribed when oral corticosteroids are planned for over 3 months (NICE CG146). Hypogonadism in men (testosterone deficiency from hypogonadism, orchidectomy, or androgen deprivation therapy for prostate cancer) causes significant trabecular bone loss. Hyperthyroidism (excessive thyroid hormone increases bone turnover); hyperparathyroidism (PTH stimulates osteoclastic bone resorption — primary hyperparathyroidism is the most common cause of hypercalcaemia in outpatients; secondary hyperparathyroidism from vitamin D deficiency in osteomalacia is distinct). Malabsorption syndromes (coeliac disease, Crohn's disease, bariatric surgery) — impair calcium and vitamin D absorption. Anorexia nervosa: profound oestrogen deficiency plus undernutrition causes severe rapid bone loss, often irreversible. Anticonvulsants (phenytoin, carbamazepine, phenobarbitone): induce hepatic CYP450 enzymes accelerating vitamin D catabolism. Risk factors: female sex, age above 65, BMI below 19 kg/m², family history of hip fracture, prior fragility fracture (2-10x increased risk of further fracture), smoking (1.2x increased hip fracture risk), alcohol above 3 units/day, long-term corticosteroid use, immobility, and low calcium/vitamin D intake.

Osteoporosis itself produces no symptoms — it is a clinically silent condition until a fragility fracture occurs, and in many patients remains unrecognised until a hip or vertebral fracture prompts investigation. The disease is therefore often described as the 'silent thief of bone.' Fragility fractures — fractures occurring from minimal trauma equivalent to or less than a fall from standing height — are the defining clinical events of osteoporosis: vertebral compression fractures: the most common osteoporotic fracture — approximately 700,000 occur per year in the United States alone; can occur spontaneously or with minimal exertion (coughing, bending, lifting a light object); cause acute severe back pain localised to the affected vertebral level, height loss (2-4cm per fracture episode), and progressive thoracic kyphosis ('Dowager's hump') with abdominal protrusion; 30% are asymptomatic at the time ('silent fractures') and are detected only on imaging; multiple vertebral fractures cause pulmonary restriction (reduced FVC from thoracic cage deformity) and gastrointestinal symptoms (early satiety, reflux from abdominal compression). Hip fractures (proximal femoral fractures — femoral neck or intertrochanteric): the most clinically severe and economically costly osteoporotic fracture — 70,000 occur annually in the UK; present with pain and deformity of the hip and inability to weight-bear after a fall; 30-day mortality is approximately 10%; 1-year mortality is 20-30% (from pneumonia, PE, cardiac events, and complications of prolonged hospitalisation); 50% of survivors never regain their pre-fracture level of mobility or independence. Wrist fractures (Colles fracture — distal radius): typically occur from a fall on an outstretched hand — a common fragility fracture that often serves as the sentinel fracture before hip or vertebral fractures occur; every wrist fragility fracture should trigger osteoporosis investigation and treatment in women over 45 years. Rib fractures (from coughing or minimal trauma), humerus fractures, and pelvis fractures are also osteoporotic fragility fractures.

DEXA scan (dual-energy X-ray absorptiometry): the gold standard for measuring bone mineral density (BMD) — measures g/cm² at the lumbar spine (L1-L4) and proximal femur (total hip and femoral neck); WHO T-score classification: normal T-score above -1.0; osteopenia T-score -1.0 to -2.5; osteoporosis T-score at or below -2.5; severe osteoporosis T-score below -2.5 with one or more fragility fractures. In younger premenopausal women and men under 50, Z-score (comparison to age-matched controls) is more appropriate — Z-score below -2.0 indicates BMD below expected range. FRAX (fracture risk assessment tool — WHO, Sheffield): integrates 12 clinical risk factors (age, sex, BMI, prior fracture, parental hip fracture, current smoking, alcohol, rheumatoid arthritis, secondary osteoporosis, glucocorticoid use) with or without femoral neck BMD to calculate 10-year probability of major osteoporotic fracture (MOF) and hip fracture — treatment thresholds are age-dependent (NICE and NOGG guidance use age-specific FRAX MOF thresholds). FRAX should be calculated before DEXA in all patients with clinical risk factors to determine who needs BMD measurement and treatment. Blood investigations to exclude secondary causes (mandatory at first assessment): serum calcium and adjusted calcium (hyperparathyroidism, malignancy); phosphate; ALP (elevated in Paget's disease, metastases, or healing fractures); 25-OH vitamin D (deficiency ubiquitous in osteoporosis patients — supplement before or alongside treatment); PTH (primary hyperparathyroidism); TSH (hyperthyroidism); full blood count (myeloma — anaemia, high ESR); serum protein electrophoresis (SPEP) and urine Bence-Jones protein (myeloma); renal function (CKD); LFTs (chronic liver disease); testosterone and LH/FSH in men (hypogonadism). Vertebral fracture assessment (VFA): low-dose lateral spine X-ray or DXA-based VFA — identifies silent vertebral deformities not detected clinically; a morphometric vertebral fracture doubles the treatment indication regardless of T-score.

Osteoporosis treatment is stratified by fracture risk and combines universal bone health support with pharmacological therapy for those at elevated fracture risk. Universal measures (all patients): adequate calcium intake (1000-1200mg/day — ideally from dietary sources including dairy, fortified foods, leafy greens; supplementation of 500-1000mg daily if dietary intake is insufficient); vitamin D supplementation (800-1000 IU cholecalciferol daily — higher doses of 1500-2000 IU if baseline levels below 50 nmol/L); weight-bearing and resistance exercise; fall prevention; cessation of smoking and alcohol excess. Anti-resorptive therapy (first-line): bisphosphonates are the most widely prescribed treatments — alendronate 70mg once weekly orally (taken fasting with water, remain upright for 30 minutes — risk of oesophagitis); risedronate 35mg weekly or 150mg monthly; zoledronic acid (Aclasta) 5mg IV infusion once yearly for 3 years (subcutaneous administration not required, suitable for patients unable to tolerate oral bisphosphonates — associated with transient flu-like reaction post-infusion). Bisphosphonates reduce vertebral fractures by 40-70% and non-vertebral fractures by 20-40%. Denosumab (Prolia, anti-RANKL monoclonal antibody): 60mg subcutaneous injection every 6 months — highly effective, particularly for those intolerant of bisphosphonates or with eGFR below 35; IMPORTANT: discontinuation without transitioning to bisphosphonate causes rapid bone loss and rebound vertebral fractures within 12-18 months — must not be stopped abruptly. Anabolic therapy for severe or treatment-resistant osteoporosis: teriparatide (recombinant PTH 1-34, 20 micrograms SC daily for 24 months — the most effective agent for increasing BMD); abaloparatide (PTH-related peptide analogue); romosozumab (Evenity, anti-sclerostin monoclonal antibody — 210mg SC monthly for 12 months, followed by anti-resorptive therapy — provides the greatest BMD increase of all approved therapies; contraindicated 12 months after myocardial infarction or stroke). Sequential treatment (anabolic followed by anti-resorptive) provides the greatest absolute fracture risk reduction in severe osteoporosis.

Hip fractures are the most devastating complication — 20-30% of patients die within 12 months from complications (aspiration pneumonia, pulmonary embolism, cardiac events, and complications of prolonged hospitalisation); 50% of survivors never regain their pre-fracture level of independence, and 20-30% require long-term institutional care. Immobility from hip fracture rapidly accelerates generalised bone loss, creating a self-reinforcing cycle of increasing fracture risk. Vertebral fracture complications: chronic disabling back pain; height loss of 2-4cm per vertebral fracture level — patients with multiple thoracic vertebral fractures may lose 10-15cm of height; severe thoracic kyphosis restricts lung expansion (spirometric restrictive pattern with reduced FVC and FRC), worsens gastro-oesophageal reflux, and causes abdominal bloating; each vertebral fracture independently increases the risk of subsequent vertebral (5x higher in the following year after incident fracture — the 'fracture cascade') and hip fracture. Bisphosphonate-related complications: osteonecrosis of the jaw (ONJ) — exposed necrotic bone in the jaw not healing after 8 weeks, particularly after invasive dental procedures (extraction, implants) in patients on bisphosphonates; more common with IV bisphosphonates (zolendronic acid for cancer — 1-12%) than oral bisphosphonates for osteoporosis (1:10,000-1:100,000); atypical subtrochanteric or femoral shaft fractures (AFF): spontaneous or minimal trauma fractures through the lateral cortex of the femur, associated with prolonged bisphosphonate therapy above 5 years; requires stopping bisphosphonate immediately and switching to teriparatide. Sequential fractures and cascade effect: one vertebral fracture increases the 1-year risk of further vertebral fracture by 5-fold (vertebral fracture cascade) — aggressive treatment and close monitoring after any first fracture is essential.

Building and maintaining peak bone mass: adequate calcium intake (UK RNI 700mg/day adults — predominantly from dairy, fortified foods, and leafy vegetables; supplementation 500-1000mg/day calcium carbonate or calcium citrate when dietary intake is insufficient); vitamin D (deficiency is extremely common in the UK — supplement 400-800 IU/day for general prevention; higher doses 800-2000 IU/day for those at high fracture risk, housebound, or in care homes); regular weight-bearing exercise throughout life — walking, running, dancing, and resistance training stimulate osteoblast activity and build cortical and trabecular bone density; avoidance of smoking (reduces oestrogen levels) and excessive alcohol (directly inhibits osteoblasts). NICE CG146 — glucocorticoid-induced osteoporosis: all adults starting oral prednisolone above 7.5mg/day for 3 months or more should receive calcium and vitamin D supplementation plus bisphosphonate (alendronate 70mg weekly first-line; if intolerant — risedronate or zolendronic acid); BMD should be measured at baseline and 1-2 years. Fall prevention: identifies and addresses intrinsic risks (visual impairment, postural hypotension, neuropathy, muscle weakness — balance and strength exercises, Tai Chi reduces falls by 30-40%) and extrinsic risks (home hazard modification — remove rugs, install grab rails, adequate lighting, non-slip bathroom surfaces); medication review (reduce or stop psychotropic medications, antihypertensives causing postural hypotension, and long-acting benzodiazepines). Post-fracture care — Fracture Liaison Service (FLS): every patient presenting with a fragility fracture should be automatically referred to an FLS (orthogeriatric-led or specialist nurse-led programme) for DEXA, FRAX calculation, secondary cause exclusion, and same-day initiation of appropriate pharmacotherapy — reduces re-fracture rates by 30-40% and is cost-effective.

See a GP for: any fracture occurring from minimal trauma or a low-energy fall (fracture from standing height or less — 'fragility fracture') — this is a clinical diagnosis of osteoporosis requiring treatment regardless of DEXA scan result; back pain associated with height loss or new thoracic kyphosis (possible vertebral compression fractures — may require urgent imaging); or if you are at high risk of osteoporosis (post-menopausal women over 65, all women over 70, men over 75, prolonged corticosteroid use, prior fragility fracture, chronic conditions such as rheumatoid arthritis, coeliac disease, or inflammatory bowel disease). Seek urgent assessment for: acute severe back pain after a fall, particularly in older adults (possible vertebral fracture requiring imaging — spinal cord compression is rare but must be excluded if associated with leg weakness or bladder dysfunction). FRAX risk calculation (WHO fracture risk assessment tool) should be used to stratify treatment decisions — a 10-year major osteoporotic fracture probability above 20% typically indicates bisphosphonate treatment. Do not wait until a fracture occurs to address osteoporosis risk.