Abstract

Summary Background and objectives: The Wnt pathway and its inhibitors (sclerostin and Dkk-1) have a primary role in the regulation of bone mass and osteoblastogenesis. The objective of this study was to analyse the effect of treatment with glucocorticoids (GCC) on the inhibitors of the Wnt pathway and their relationship with bone mass and the parameters for bone turnover. Methods: A transverse study including 15 patients (9 women and 6 men) with an mean age of 51±21 years at the start of treatment with GCC (≥7.5 mg/day, ≤6 months). Levels of sclerostin, blood Dkk-1 and blood markers for bone turnover (procollagen 1 N-terminal propeptide [P1NP], osteocalcin [OC], and carboxyterminal telopeptide of collagen type 1 [CTX] ) were determined, and bone densitometry ( DXA) in the lumbar spine was carried out, in all patients. The results were compared with a control group. Results: The mean dose of glucocorticoids was 58±21 mg/day, in the majority of patients (73%) indicated by idiopathic thrombocytopenic purpura. The patients treated with glucocorticoids had a reduction in the parameters for bone formation compared with a control group (OC: 7.4±2.8 vs 24.4±6.2 ng/ml, p<0.01) and a reduction in blood Dkk-1 (29.6±23.6 vs 48.3±15.6 pmol/L, p=0.02). No significant differences were observed in values for blood sclerostin, although this correlated positively with the dose of GCC received and lumbar bone mineral density. Conclusion: Contrary to what is seen in experimental studies, the start of treatment with glucocorticoids is associated with a reduction in blood levels of Dkk-1. These results indicate the necessity of analysing these inhibitors and their relationship with remodelling and bone mass during this process over the long term.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.