Abstract

PTH is a key regulator of bone structure and remodeling. When PTH is absent in hypoparathyroidism (HypoPT), bone mass is increased and remodeling is decreased. In addition to bone structure and remodeling, bone material properties contribute to fracture resistance. Yet little is known about the relationship between PTH and bone material properties. Impact microindentation provides a clinical assessment of microfracture resistance, measured as the bone material strength index (BMSi). Case-control cross-sectional study of PTH levels and in vivo BMSi measurement by impact microindentation at the anterior tibia in HypoPT patients (n = 17) and in controls matched for age, sex, and menopausal status (n = 17), with follow-up in a subgroup of HypoPT patients (n = 5) after recombinant human parathyroid hormone (1-84) [rhPTH(1-84)] treatment. BMSi was positively associated with PTH levels in controls (r = 0.58, p = 0.02) and was 11% lower (p = 0.01) in HypoPT patients as compared with controls. In HypoPT, lower BMSi was associated with a trend toward greater supplemental calcium doses (p = 0.07). BMSi increased after rhPTH(1-84) treatment in the HypoPT patients who underwent repeat microindentation. PTH levels might be associated with bone material strength, although other factors might be contributory. In HypoPT, resistance to microfracture is decreased and may be associated with greater supplemental calcium doses and might increase with PTH replacement. It remains to be determined whether changes in bone remodeling and microarchitecture contribute to the effects of PTH on microfracture resistance.

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