Residency · Residency · Physical Medicine Rehabilitation
Osteoporosis and Fragility Fracture Prevention in Rehabilitation
Introduction
Osteoporosis is a systemic skeletal disease characterized by low bone mass and microarchitectural deterioration, resulting in increased bone fragility and fracture risk. Rehabilitation populations carry an exceptionally high osteoporosis burden due to immobilization, neurological injury, medication effects, and nutritional deficits. Physiatrists are well positioned to identify at-risk patients, initiate diagnostic evaluation, implement pharmacological and non-pharmacological interventions, and design safe exercise programs that reduce fracture risk.
Epidemiology
Affects an estimated 200 million people worldwide; 10.2 million Americans over 50 have osteoporosis. Fragility fractures: occur from a fall from standing height or less; 2 million annually in the United States. Hip fractures carry the highest morbidity: 20-30% one-year mortality, 50% never return to prior functional level. Vertebral compression fractures are the most common osteoporotic fracture; 70% are clinically unrecognized.
Sublesional osteoporosis in SCI: bone mineral density declines 25-50% in the first 2 years below the level of injury; fracture risk increases 2-3 fold. Post-stroke hemiosteoporosis: paretic limb bone loss begins within weeks of stroke onset.
Pathophysiology of Bone Loss
Bone remodeling is a continuous process of osteoclast-mediated resorption and osteoblast-mediated formation. Osteoporosis results from an imbalance favoring resorption over formation. RANK/RANKL/OPG pathway: RANKL activates osteoclasts via RANK receptor; osteoprotegerin (OPG) is a decoy receptor that inhibits this activation. Mechanical loading (Wolff's Law): bone adapts to the loads placed upon it; removal of mechanical stress (immobilization, paralysis, microgravity) causes rapid bone loss.
Estrogen deficiency (postmenopausal): accelerated bone resorption due to loss of estrogen's inhibitory effect on osteoclasts. Glucocorticoid-induced osteoporosis: directly suppresses osteoblast function, enhances osteoclast survival, and impairs calcium absorption.
Risk Factors in Rehabilitation Populations
Immobilization and non-weight-bearing: bed rest causes 1-2% bone loss per week in the first 6 weeks. Spinal cord injury: most rapid sublesional bone loss occurs in the first 12-18 months; distal femur and proximal tibia are highest fracture risk sites. Stroke: paretic limb osteoporosis; compounded by falls risk and impaired protective reflexes. Traumatic brain injury: hormonal disruption (hypopituitarism), prolonged immobilization.
Medication effects: chronic corticosteroids, anticonvulsants (phenytoin, carbamazepine), heparin, proton pump inhibitors, aromatase inhibitors. Nutritional deficits: vitamin D deficiency (prevalent in 50-80% of rehabilitation patients), inadequate calcium and protein intake. Chronic disease: rheumatoid arthritis, COPD, diabetes, chronic kidney disease.
Diagnostic Evaluation
Dual-Energy X-Ray Absorptiometry (DXA)
Gold standard for diagnosing osteoporosis and monitoring treatment response. Measures bone mineral density (BMD) at lumbar spine, femoral neck, and total hip. T-score interpretation: normal (greater than -1.0), osteopenia (-1.0 to -2.5), osteoporosis (-2.5 or less). Screening recommended for all women 65 and older, men 70 and older, and younger patients with risk factors. In SCI, DXA of the distal femur and proximal tibia may be more informative than standard hip and spine measurements.
| T-Score | Classification | Fracture Risk | Management |
|---|---|---|---|
| > -1.0 | Normal | Low | Lifestyle measures |
| -1.0 to -2.5 | Osteopenia | Moderate | FRAX assessment; consider treatment if high risk |
| ≤ -2.5 | Osteoporosis | High | Pharmacologic treatment indicated |
| ≤ -2.5 + fracture | Severe osteoporosis | Very high | Aggressive treatment, fall prevention |
FRAX Tool
Fracture Risk Assessment Tool: estimates 10-year probability of major osteoporotic fracture and hip fracture. Incorporates BMD with clinical risk factors: age, sex, BMI, prior fracture, parental hip fracture, glucocorticoid use, rheumatoid arthritis, smoking, alcohol intake. Treatment threshold: 10-year hip fracture risk of 3% or greater, or major osteoporotic fracture risk of 20% or greater.
Laboratory Evaluation
Serum calcium, phosphorus, magnesium, 25-hydroxyvitamin D, PTH. Comprehensive metabolic panel, CBC, thyroid function. Bone turnover markers: serum CTX (resorption), P1NP (formation); useful for monitoring treatment response. Consider secondary causes: serum protein electrophoresis, celiac antibodies, 24-hour urine calcium, cortisol.
Non-Pharmacological Management
Exercise
Weight-bearing exercise: walking, stair climbing, dancing; stimulates bone formation at loaded sites. Resistance training: progressive loading improves BMD at the spine and hip; 2-3 sessions per week. Balance training: Tai Chi, single-leg stance, perturbation training; reduces falls risk by 20-30%. Impact exercise: jumping, hopping (when safe); most osteogenic stimulus; not appropriate for all rehabilitation patients.
Exercise prescription must account for fracture risk, balance impairment, and fall history; avoid high-risk activities in severely osteoporotic patients (heavy spinal flexion loading, high-impact activities).
Nutritional Optimization
Calcium: 1000-1200 mg daily (diet plus supplementation); dairy, fortified foods, leafy greens. Vitamin D: 800-2000 IU daily; target serum 25(OH)D level of 30-50 ng/mL; higher doses may be needed initially to correct deficiency. Protein: adequate intake (1.0-1.2 g/kg/day) supports bone matrix and muscle health. Avoid excess alcohol (greater than 3 drinks/day) and smoking cessation.
Fall Prevention
Multifactorial risk assessment and intervention (see Lecture 72). Home safety assessment and modification. Vision correction, medication review, assistive device optimization. Hip protectors for high-risk institutionalized patients.
Pharmacological Treatment
Antiresorptive Agents
Bisphosphonates: first-line therapy; inhibit osteoclast activity. Alendronate 70 mg weekly PO; risedronate 35 mg weekly PO. Zoledronic acid 5 mg IV annually (preferred when oral adherence is challenging or GI issues present). Reduce hip fracture risk by 40-50% and vertebral fracture risk by 50-70%.
Drug holiday after 3-5 years of oral or 3 years of IV therapy in non-high-risk patients. Denosumab: monoclonal antibody against RANKL; 60 mg SC every 6 months. Does not require renal dosing; safe in CKD. Rapid rebound bone loss and vertebral fracture risk upon discontinuation; must transition to bisphosphonate.
Anabolic Agents
Teriparatide (PTH 1-34): 20 mcg SC daily for up to 2 years; stimulates osteoblast activity. Abaloparatide (PTHrP analog): 80 mcg SC daily; similar mechanism to teriparatide. Romosozumab: monoclonal antibody against sclerostin; 210 mg SC monthly for 12 months; dual action (anabolic and antiresorptive); cardiovascular risk warning. Anabolic agents are reserved for severe osteoporosis, patients with fractures despite bisphosphonate therapy, or very high fracture risk. Must be followed by antiresorptive therapy to maintain bone gains.
Special Populations
Glucocorticoid-induced osteoporosis: initiate bisphosphonate if prednisone 2.5 mg or more daily for 3 months or longer; calcium and vitamin D mandatory. SCI: limited evidence for pharmacological prevention of sublesional osteoporosis; bisphosphonates may slow but not prevent bone loss; functional electrical stimulation (FES) cycling under investigation. Premenopausal women: treat underlying cause; bisphosphonates used cautiously given long skeletal half-life and teratogenic potential.
Fragility Fracture Management in Rehabilitation
Vertebral compression fractures: pain management (analgesics, bracing with thoracolumbar orthosis), early mobilization, physical therapy; vertebroplasty or kyphoplasty for refractory pain. Hip fractures: surgical fixation followed by intensive rehabilitation; early weight-bearing as tolerated per surgical team. Distal radius fractures: splinting/casting, hand therapy, fall prevention assessment. Every fragility fracture is an opportunity to initiate osteoporosis evaluation and treatment; the "fracture liaison service" model reduces secondary fracture rates by 30-40%.
Key Clinical Pearls
Every fragility fracture should trigger osteoporosis evaluation and treatment; the greatest predictor of future fracture is a prior fragility fracture. Vitamin D deficiency is nearly universal in rehabilitation populations; screen and supplement aggressively (target 30-50 ng/mL). In SCI, standard DXA sites (spine and hip) may underestimate fracture risk; distal femur and proximal tibia are the highest-risk locations for fracture. Denosumab discontinuation causes rapid rebound bone loss and vertebral fracture risk; always transition to a bisphosphonate before stopping. Weight-bearing exercise and resistance training are the most effective non-pharmacological interventions for bone health; prescribe them as deliberately as medications.
References
- Cosman F, de Beur SJ, LeBoff MS, et al. Clinician's guide to prevention and treatment of osteoporosis. Osteoporosis International. 2014;25(10):2359-2381.
- Carbone LD, Chin AS, Burns SP, et al. Mortality after lower extremity fractures in men with spinal cord injury. Journal of Bone and Mineral Research. 2014;29(2):432-439.
- Lyles KW, Colon-Emeric CS, Magaziner JS, et al. Zoledronic acid and clinical fractures and mortality after hip fracture. New England Journal of Medicine. 2007;357(18):1799-1809.
- Shoback D, Rosen CJ, Black DM, et al. Pharmacological management of osteoporosis in postmenopausal women: an Endocrine Society guideline update. Journal of Clinical Endocrinology & Metabolism. 2020;105(3):587-594.