Romagnoli, Elisabetta; Carnevale, Vincenzo
Parathyroid hormone (PTH) action induces catabolic and anabolic skeletal effects. The continuous exposure of osteoblasts and osteocytes to PTH activates osteoclasts activity through the OPG-RANKL-RANK pathway. The enhanced bone formation mostly depends on the inhibition of sclerostin, an antagonist of the Wnt/β-catenin signalling.Nowadays, the hallmark of primary hyperparathyroidism (PHPT), also in patients with minimal clinical manifestations, is the increased bone turnover rate, which translates in a preferential loss of cortical tissue with relative preservation of the trabecular bone. The current guidelines recommend areal bone mineral density (aBMD) assessment of the distal radius, lumbar spine, total hip and femoral neck, by dual-energy X-ray absorptiometry (DXA), every 1–2 years. Parathyroidectomy is indicated in postmenopausal women and men ≥50 years having a T-score ≤−2.5. DXA results do not fully explain the increased risk of fractures in PHPT, postmenopausal patients showing a higher vertebral fracture rate even with preserved BMD. High-resolution peripheral quantitative computed tomography (HR-pQCT) separately measures the true volumetric density (vBMD) of cortical and trabecular compartments, both decreased in PHPT. Trabecular bone score (TBS) indirectly estimates trabecular microarchitecture and correlates to μCT findings and to HR-pQCT-measured total, cortical, trabecular vBMD. Low TBS values are found also in patients with normal aBMD of the lumbar spine.In hypoparathyroidism, the absent or inappropriately low serum PTH levels associate to BMD values above the average at the lumbar spine and femur, whereas TBS is unchanged. Long-term administration of rhPTH 1-84 stimulates bone remodelling and increases aBMD at the lumbar spine and femoral neck while decreases it at the distal radius. rhPTH 1-84 also promotes a transient increase in trabecular strength, whose effects on fracture risk are uncertain.