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dc.contributor.authorDelgado Calle, Jesús
dc.contributor.authorArozamena García, Jana
dc.contributor.authorGarcía Renedo, Raúl Javier 
dc.contributor.authorGarcía Ibarbia, María del Carmen 
dc.contributor.authorPascual Carra, Asunción 
dc.contributor.authorGonzález Macías, Jesús 
dc.contributor.authorRiancho Moral, José Antonio 
dc.contributor.otherUniversidad de Cantabriaes_ES
dc.date.accessioned2015-04-22T06:08:44Z
dc.date.available2015-04-22T06:08:44Z
dc.date.issued2011-10
dc.identifier.issn0171-967X
dc.identifier.urihttp://hdl.handle.net/10902/6240
dc.description.abstractOsteocytes play a central role in the regulation of bone remodeling. The aim of this study was to explore osteocyte function, and particularly the expression of SOST, a Wnt inhibitor, in patients with hip fractures. Serum sclerostin levels were measured by ELISA. The expression of several osteocytic genes was studied by quantitative PCR in trabecular samples of the femoral head of patients with hip fractures, hip osteoarthritis and control subjects. The presence of sclerostin protein and activated caspase 3 was revealed by immunostaining. There were no significant differences in serum sclerostin between the three groups. Patients with fractures have fewer lacunae occupied by osteocytes (60 ± 5% vs. 64 ± 6% in control subjects, P = 0.014) and higher numbers of osteocytes expressing activated caspase 3, a marker of apoptosis. The proportion of sclerostin-positive lacunae was lower in patients with fractures than in control subjects (34 ± 11% vs. 69 ± 10%, P = 2 × 10(-8)). The proportion of sclerostin-positive osteocytes was also lower in patients. RNA transcripts of SOST, FGF23 and PHEX were also less abundant in fractures than in control bones (P = 0.002, 5 × 10(-6), and 0.04, respectively). On the contrary, in patients with osteoarthritis, there was a decreased expression of SOST and FGF23, without differences in PHEX transcripts or osteocyte numbers. Osteocyte activity is altered in patients with hip fractures, with increased osteocyte apoptosis and reduced osteocyte numbers, as well as decreased transcription of osteocytic genes. Therefore, these results suggest that an osteocyte deficiency may play a role in the propensity to hip fractures.es_ES
dc.format.extent24 p.es_ES
dc.language.isoenges_ES
dc.publisherSpringer Verlages_ES
dc.rights© Springer Verlag. The final publication is available at Springer via http://dx.doi.org/10.1007/s00223-011-9522-0es_ES
dc.sourceCalcified Tissue International. 2011 Oct;89(4):327-34es_ES
dc.titleOsteocyte deficiency in hip fractureses_ES
dc.typeinfo:eu-repo/semantics/articlees_ES
dc.relation.publisherVersionhttp://link.springer.com/article/10.1007%2Fs00223-011-9522-0es_ES
dc.rights.accessRightsopenAccesses_ES
dc.identifier.DOI10.1007/s00223-011-9522-0
dc.type.versionacceptedVersiones_ES


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