{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,24]],"date-time":"2026-04-24T15:54:26Z","timestamp":1777046066745,"version":"3.51.4"},"reference-count":25,"publisher":"FapUNIFESP (SciELO)","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Arq Bras Endocrinol Metab"],"published-print":{"date-parts":[[2014,7]]},"abstract":"<jats:p>Hypoparathyroidism is a rare disorder that may be acquired or inherited. Postsurgical hypoparathyroidism is responsible for the majority of acquired hypoparathyroidism. Bone disease occurs in hypoparathyroidism due to markedly reduced bone remodeling due to the absence or low levels of parathyroid hormone. Chronically reduced bone turnover in patients with hypoparathyroidism typically leads to higher bone mass than in age- and sex-matched controls. Whether this increased bone density reduces fracture risk is less certain, because while increased bone mineralization may be associated with increased brittleness of bone, this does not appear to be the case in hypoparathyroidism. Treatment of hypoparathyroidism with recombinant parathyroid hormone may reduce bone mineral density but simultaneously strengthen the mechanical properties of bone.<\/jats:p>","DOI":"10.1590\/0004-2730000003399","type":"journal-article","created":{"date-parts":[[2014,8,20]],"date-time":"2014-08-20T18:56:51Z","timestamp":1408561011000},"page":"545-552","source":"Crossref","is-referenced-by-count":26,"title":["Bone disease in hypoparathyroidism"],"prefix":"10.1590","volume":"58","author":[{"given":"Bart L.","family":"Clarke","sequence":"first","affiliation":[{"name":"Mayo Clinic College of Medicine,  United States"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"530","reference":[{"key":"ref1","doi-asserted-by":"crossref","first-page":"391","DOI":"10.1056\/NEJMcp0803050","article-title":"Clinical practice. 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