Disruption of glucocorticoid signaling in chondrocytes delays metaphyseal fracture healing but does not affect normal cartilage and bone development

States of glucocorticoid excess are associated with defects in chondrocyte function. Most prominently there is a reduction in linear growth but delayed healing of fractures that require endochondral ossification to also occur. In contrast, little is known about the role of endogenous glucocorticoids...

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Publicado no:Bone
Main Authors: Tu, Jinwen, Henneicke, Holger, Zhang, Yaqing, Stoner, Shihani, Cheng, Tegan L., Schindeler, Aaron, Chen, Di, Tuckermann, Jan, Cooper, Mark S., Seibel, Markus J., Zhou, Hong
Formato: Artigo
Idioma:Inglês
Publicado em: 2014
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Article
Acesso em linha:https://ncbi.nlm.nih.gov/pmc/articles/PMC4284102/
https://ncbi.nlm.nih.gov/pubmed/25193158
https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1016/j.bone.2014.08.016
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