Approach to the patient: management of bone fragility in patients with chronic hypoparathyroidism

Parathyroid hormone (PTH) is the main hormonal regulator of bone remodeling; thus, chronic hypoparathyroidism (HypoPT) leads to low bone turnover that might compromise bone strength, despite the normal or even high bone mineral density. Recent studies suggest that fracture risk might be increased in patients with HypoPT. Given that all available treatments for osteoporosis affect bone remodeling, management of bone fragility of any etiology in patients with HypoPT is challenging and lacks clinical evidence in terms of fracture risk reduction. In the present article we describe the changes in bone remodeling and bone strength in patients with chronic HypoPT managed by conventional therapy and under PTH-replacement. In addition, based on pathophysiology and the limited existing evidence, we discuss which osteoporosis medication could be used in patients with HypoPT and concurrent increased bone fragility. In HypoPT patients under conventional treatment with calcium and active vitamin D, administration of potent antiresorptives (bisphosphonates, denosumab) should be done under close monitoring, given their antiremodeling action that might result in hypocalcemia, while the effect on bone material properties is not known. Teriparatide is probably the best available option, at least in the short-term. In contrast, patients with HypoPT on long-term PTH replacement therapy who experience fragility fractures, should probably be treated with antiresorptives, although the optimal therapeutic regimen, in terms of safety and efficacy, is yet unknown.