Abstract
Hypocalcemia and hypophosphatemia are common complications after parathyroidectomy (PTX). Sudden removal of high circulating levels of parathyroid hormone (PTH) causes decreased osteoclastic resorption resulting in a decreased bone remodeling space. These phenomena are likely due to an increased influx of calcium and phosphorus into bone. However, there are currently no data to support this hypothesis. In this study, we found that PTX significantly reduced levels of PTH, calcium and phosphate. Compared with preoperative levels, after 1 year, postoperative PTH, calcium and phosphate levels were 295.6 ± 173.7 pg/mL (P < 0.05), 86.62 ± 15.98 mg/dL (P < 0.05) and 5.56 ± 2.03 mg/dL (P < 0.05), respectively. We investigated continuous bovine PTH administration as well as withdrawal of bovine PTH stimulation in the mouse osteoblast precursor cell line MC3T3-E1. MC3T3-E1 cells were cultured with continuous bovine PTH treatment for 20 days or with transient bovine PTH treatment for 10 days. High doses of continuous bovine PTH exposure strongly reduced cell proliferation, alkaline phosphatase activity and the number of mineralized calcium nodules. However, withdrawal of bovine PTH (100 ng/mL) significantly increased the number of mineralized calcium nodules and caused a rapid decline in calcium and phosphorus content of culture medium. In conclusion, continuous exposure to bovine PTH inhibited osteoblast differentiation and reduced the formation of mineralized nodules. However, this inhibition was removed and mineralized nodule formation resumed with withdrawal of bovine PTH. According to the results of our clinical examinations and in vitro experiments, we hypothesize that the sudden removal of high levels of PTH may cause an increased influx of calcium and phosphorus into bone after PTX.
Highlights
Since parathyroid hormone analogs become the only US FDA-approved anabolic drug, intermittent parathyroid hormone has been widely used in clinic to treat bone loss due to conditions such as osteoporosis that increases bone formation by osteoblasts.[1]
Bone mass and turnover are maintained by the coordinated balance between bone formation by osteoblasts and bone resorption by osteoclasts, under the control of many cytokines. [10,11] Osteoclasts are multinucleated cells which arise from fusion of bone marrow monocytes and macrophages that are specialized to carry out bone resorption, whereas osteoblasts are responsible for osteogenesis.[12]
In order to clarify the mechanism of hypocalcaemia and hypophosphatemia in these patients, we examined the impact of parathyroid hormone (PTH) of the osteoblastic cell line MC3T3-E1
Summary
Since parathyroid hormone analogs become the only US FDA-approved anabolic drug, intermittent parathyroid hormone (iPTH) has been widely used in clinic to treat bone loss due to conditions such as osteoporosis that increases bone formation by osteoblasts.[1] PTH increases osteoblastogenesis and osteoblast maturation, promotes osteoblast survival and inhibits osteoblast apoptosis, thereby increasing osteoblast number and function.[2,3] A low dose and intermittently PTH seems to be able to exert positive effects on bone volume and microarchitecture. Bone mass and turnover are maintained by the coordinated balance between bone formation by osteoblasts and bone resorption by osteoclasts, under the control of many cytokines. In chronic kidney disease (CKD) patients with secondary hyperparathyroidism (SHPT), continuous elevation of parathyroid hormone (PTH) increases osteoclast activity, stimulates bone resorption, mobilizes bone calcium, and disrupts the balance between osteoclasts and osteoblasts
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