Effects of an Excess and a Deficiency of Endogenous Parathyroid Hormone on Volumetric Bone Mineral Density and Bone Geometry Determined by Peripheral Quantitative Computed Tomography in Female Subjects

Peripheral quantitative computed tomography (pQCT) is useful for evaluating volumetric bone mineral density (vBMD) as well as bone mineral density (BMD) of cortical and trabecular bones separately. Although PTH affects cortical and trabecular bones differently, the effects of endogenous PTH on vBMD and bone geometry have not previously been examined with pQCT. We, therefore, investigated the effects of an excess and a deficiency of endogenous PTH on bone by employing dual-energy x-ray absorptiometry and pQCT in 36 female patients with primary hyperparathyroidism (hyper), nine female patients with idiopathic or postoperative hypoparathyroidism (hypo), and 100 normal controls matched to age, gender, and body size (cont). Lumbar BMD by dual-energy x-ray absorptiometry was higher in the order: hypo > cont = hyper, and radius-1/3 BMD was significantly higher in the order: hypo > cont > hyper. The area of radius-1/3 was significantly higher in hyper than in cont. As for pQCT, trabecular vBMD was significantly higher in the order: hypo > cont > hyper at the 4% site (hypo, 157.5 ± 36.7 mg/cm3; cont, 123.4 ± 47.5 mg/cm3; hyper, 98.4 ± 41.7 mg/cm3). Cortical vBMD was higher in the order: hypo > cont > hyper at the 20% site (hypo, 1141.1 ± 53.1 mg/cm3; cont, 1090.2 ± 72.9 mg/cm3; hyper, 1038.6 ± 89.1 mg/cm3). Total bone area and endosteal and periosteal circumferences were significantly higher in hyper than in cont and hypo. Cortical area and thickness were higher in the order: hypo > cont > hyper. Bone strength indices were not significantly different among the three groups. In conclusion, vBMD evaluation revealed that an excess of endogenous PTH was catabolic for both cortical and trabecular bones, and that bone mass (especially trabecular bone mass) was preserved under a condition of deficient endogenous PTH. An excess of endogenous PTH stimulated periosteal bone formation, which might partly compensate for a decrease in bone strength induced by low BMD.