Increased vertebral morphometric fracture in patients with postsurgical hypoparathyroidism despite normal bone mineral density

Background The mechanism behind parathyroid hormone (PTH) activation of bone remodeling is intimately dependent on the time of exposure of bone cells to hormone levels. Sustained high PTH levels trigger catabolism, while transitory elevations induce anabolism. The effects of hypoparathyroidism (PhPT) on bone are unknown. The objective was to study the impact of PhPT on bone mineral density (BMD), on the frequency of subclinical vertebral fracture and on mandible morphometry.