A 45-year-old woman with primary hyperparathyroidism undergoes a DEXA scan. T-score at lumbar spine is −3.2 and at femoral neck −2.8. She sustains a low-energy distal radius fracture. What is the orthopedic implication regarding fracture healing in the setting of primary hyperparathyroidism?
- A Fracture healing is accelerated because PTH has direct osteoanabolic effects
- B Fracture healing is delayed because chronic PTH excess causes predominantly osteoclastic activity and impaired callus mineralisation ✓
- C Fracture healing proceeds normally; hyperparathyroidism affects bone density but not repair
- D Fracture healing is unaffected; only renal function determines calcium balance
Explanation
Chronic continuous excess PTH (as in primary hyperparathyroidism) causes predominantly osteoclastic bone resorption (cortical bone loss), subperiosteal bone resorption (radial border of middle phalanx — classic sign), and salt-and-pepper skull on X-ray. Unlike intermittent PTH (which is anabolic as in teriparatide), continuous excess PTH leads to impaired bone mineralization, fibrous replacement (osteitis fibrosa cystica), and delayed/impaired fracture healing due to poor bone quality and abnormal calcium-phosphate balance. Fracture healing in hyperparathyroidism is therefore delayed. This is the mechanistic basis for needing parathyroidectomy before elective fracture fixation in severe cases.
Reference: Maheshwari Essential Orthopaedics, 6th ed.
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Written and medically reviewed by the StethoPrep medical team.