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Article summary:

1. Glucocorticoids (GCs) disrupt skeletal angiogenesis by reducing the production of platelet-derived growth factor BB (PDGF-BB) in preosteoclasts.

2. GCs reduce the binding of NF-κB to the Pdgfb promoter, leading to decreased PDGF-BB transcription and reduced H-type vessel formation.

3. Longer exposure to GCs leads to decreased POC numbers, H-type vessels, bone formation rate, bone volume, and bone length.

Article analysis:

The article is generally reliable and trustworthy as it provides a detailed description of the research conducted and its results. The authors have provided evidence for their claims through experiments conducted both in vivo and in vitro, which supports their conclusions that glucocorticoids disrupt skeletal angiogenesis through transrepression of NF-κB mediated preosteoclast PDGF-BB transcription in young mice.

However, there are some potential biases that should be noted. Firstly, the study only focuses on the effects of glucocorticoids on skeletal angiogenesis in young mice; thus, it does not explore any potential effects on other age groups or species. Secondly, while the authors provide evidence for their claims from experiments conducted both in vivo and in vitro, they do not provide any evidence from clinical trials or studies involving human subjects; thus, further research is needed to determine if these findings can be applied to humans as well. Finally, while the authors discuss possible risks associated with glucocorticoid use such as osteoporosis and growth retardation, they do not provide any recommendations for mitigating these risks or suggest alternative treatments that may be more effective than glucocorticoid use.