{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,28]],"date-time":"2026-09-28T20:13:44Z","timestamp":1790626424019,"version":"4.1.0"},"reference-count":64,"publisher":"The Endocrine Society","issue":"12","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2012,12,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>We have previously confirmed a paradoxical mineralizing enthesopathy as a hallmark of X-linked hypophosphatemia. X-linked hypophosphatemia is the most common of the phosphate-wasting disorders mediated by elevated fibroblast growth factor 23 (FGF23) and occurs as a consequence of inactivating mutations of the PHEX gene product. Despite childhood management of the disease, these complications of tendon and ligament insertion sites account for a great deal of the disease's morbidity into adulthood. It is unclear whether the enthesopathy occurs in other forms of renal phosphate-wasting disorders attributable to high FGF23 levels. Here we describe two patients with autosomal recessive hypophosphatemic rickets due to the Met1Val mutation in dentin matrix acidic phosphoprotein 1 (DMP1). In addition to the biochemical and skeletal features of long-standing rickets with elevated FGF23 levels, these individuals exhibited severe, debilitating, generalized mineralized enthesopathy. These data suggest that enthesophytes are a feature common to FGF23-mediated phosphate-wasting disorders. To address this possibility, we examined a murine model of FGF23 overexpression using a transgene encoding the secreted form of human FGF23 (R176Q) cDNA (FGF23-TG mice). We report that FGF23-TG mice display a similar mineralizing enthesopathy of the Achilles and plantar facial insertions. In addition, we examined the impact of standard therapy for phosphate-wasting disorders on enthesophyte progression. We report that fibrochondrocyte hyperplasia persisted in Hyp mice treated with oral phosphate and calcitriol. In addition, treatment had the untoward effect of further exacerbating the mineralization of fibrochondrocytes that define the bone spur of the Achilles insertion. These studies support the need for newer interventions targeted at limiting the actions of FGF23 and minimizing both the toxicities and potential morbidities associated with standard therapy.<\/jats:p>","DOI":"10.1210\/en.2012-1551","type":"journal-article","created":{"date-parts":[[2012,10,5]],"date-time":"2012-10-05T03:23:02Z","timestamp":1349407382000},"page":"5906-5917","source":"Crossref","is-referenced-by-count":57,"title":["Mineralizing Enthesopathy Is a Common Feature of Renal Phosphate-Wasting Disorders Attributed to FGF23 and Is Exacerbated by Standard Therapy in Hyp Mice"],"prefix":"10.1210","volume":"153","author":[{"given":"Andrew C.","family":"Karaplis","sequence":"first","affiliation":[{"name":"McGill University (A.C.K., J.-P.F.), Montr\u00e9al, Qu\u00e9bec, Canada H9X 3V9"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiuying","family":"Bai","sequence":"first","affiliation":[{"name":"Lady Davis Institute for Medical Research (X.B.), Montr\u00e9al, Qu\u00e9bec, Canada H3T 1E2"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jean-Pierre","family":"Falet","sequence":"first","affiliation":[{"name":"McGill University (A.C.K., J.-P.F.), Montr\u00e9al, Qu\u00e9bec, Canada H9X 3V9"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Carolyn M.","family":"Macica","sequence":"first","affiliation":[{"name":"Yale University School of Medicine (C.M.M.), New Haven, Connecticut 06520"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"80","reference":[{"key":"2020071612133094900_B1","doi-asserted-by":"crossref","first-page":"4667","DOI":"10.1073\/pnas.73.12.4667","article-title":"Hypophosphatemia: mouse model for human familial hypophosphatemic (vitamin D-resistant) rickets.","volume":"73","author":"Eicher","year":"1976","journal-title":"Proc Natl Acad Sci USA"},{"key":"2020071612133094900_B2","doi-asserted-by":"crossref","first-page":"37419","DOI":"10.1074\/jbc.M304544200","article-title":"Regulation of fibroblastic growth factor 23 expression but not degradation by PHEX.","volume":"278","author":"Liu","year":"2003","journal-title":"J Biol Chem"},{"key":"2020071612133094900_B3","doi-asserted-by":"crossref","first-page":"977","DOI":"10.1006\/bbrc.2001.5084","article-title":"FGF-23 inhibits renal tubular phosphate transport and is a PHEX substrate.","volume":"284","author":"Bowe","year":"2001","journal-title":"Biochem Biophys Res Commun"},{"key":"2020071612133094900_B4","doi-asserted-by":"crossref","first-page":"1305","DOI":"10.1681\/ASN.2005111185","article-title":"Fibroblast growth factor 23 is a counter-regulatory phosphaturic hormone for vitamin D.","volume":"17","author":"Liu","year":"2006","journal-title":"J Am Soc Nephrol"},{"key":"2020071612133094900_B5","doi-asserted-by":"crossref","first-page":"2342","DOI":"10.1681\/ASN.2007121301","article-title":"FGFR3 and FGFR4 do not mediate renal effects of FGF23.","volume":"19","author":"Liu","year":"2008","journal-title":"J Am Soc Nephrol"},{"key":"2020071612133094900_B6","doi-asserted-by":"crossref","first-page":"2206","DOI":"10.1074\/jbc.M207872200","article-title":"Human fibroblast growth factor-23 mutants suppress Na+-dependent phosphate co-transport activity and 1\u03b1,25-dihydroxyvitamin D3 production.","volume":"278","author":"Saito","year":"2003","journal-title":"J Biol Chem"},{"key":"2020071612133094900_B7","doi-asserted-by":"crossref","first-page":"770","DOI":"10.1038\/nature05315","article-title":"Klotho converts canonical FGF receptor into a specific receptor for FGF23.","volume":"444","author":"Urakawa","year":"2006","journal-title":"Nature"},{"key":"2020071612133094900_B8","doi-asserted-by":"crossref","first-page":"492","DOI":"10.1210\/en.2009-0564","article-title":"Increased bone volume and correction of HYP mouse hypophosphatemia in the Klotho\/HYP 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