What question did this study set out to answer?

To evaluate FGF-23 expression in fibrous dysplasia bone tissue and determine its association with renal phosphate wasting in patients with fibrous dysplasia and McCune-Albright syndrome.

September 1, 2003Journal of Clinical InvestigationOpen Access

FGF-23 in fibrous dysplasia of bone and its relationship to renal phosphate wasting

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Authors

MRMara Riminucci MCMichael T. Collins NFNeal S. Fedarko

Discussion

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Overview

Translational study reveals elevated FGF-23 production in fibrous dysplasia of bone with renal phosphate wasting, indicating its causative role in mineral dysregulation.

Key Points

To evaluate FGF-23 expression in fibrous dysplasia bone tissue and determine its association with renal phosphate wasting in patients with fibrous dysplasia and McCune-Albright syndrome.
Analyzed in vivo and in vitro FGF-23 production by normal and fibrous dysplasia (FD) osteoprogenitors using in situ hybridization to localize mRNA expression.
Measured and compared circulating serum FGF-23 levels in patients with FD/McCune-Albright syndrome (FD/MAS) against age-matched normal controls.
Assessed serum FGF-23 concentrations between FD/MAS patients with versus without renal phosphate wasting, correlating levels with disease burden and bone turnover markers.
In situ hybridization identified fibrous cells, osteogenic cells, and microvascular wall cells as primary cellular sources of FGF-23 expression in FD tissue.
Serum FGF-23 concentrations were significantly elevated in FD/MAS patients compared to normal controls, with significantly higher levels in patients exhibiting renal phosphate wasting compared to those without.
Circulating FGF-23 levels correlated positively with total skeletal disease burden and bone turnover markers of disease activity.

Cite This Study

Riminucci et al. (2003) studied this question.

synapsesocial.com/papers/69daa4df00ab073a27838a43 https://doi.org/10.1172/jci18399

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September 1, 2003Journal of Clinical InvestigationOpen Access

FGF-23 in fibrous dysplasia of bone and its relationship to renal phosphate wasting

View Full Paper

Ask AI

Bookmark

Authors

MRMara Riminucci MCMichael T. Collins NFNeal S. Fedarko

Discussion

Member takes

Overview

Translational study reveals elevated FGF-23 production in fibrous dysplasia of bone with renal phosphate wasting, indicating its causative role in mineral dysregulation.

Key Points

To evaluate FGF-23 expression in fibrous dysplasia bone tissue and determine its association with renal phosphate wasting in patients with fibrous dysplasia and McCune-Albright syndrome.
Analyzed in vivo and in vitro FGF-23 production by normal and fibrous dysplasia (FD) osteoprogenitors using in situ hybridization to localize mRNA expression.
Measured and compared circulating serum FGF-23 levels in patients with FD/McCune-Albright syndrome (FD/MAS) against age-matched normal controls.
Assessed serum FGF-23 concentrations between FD/MAS patients with versus without renal phosphate wasting, correlating levels with disease burden and bone turnover markers.
In situ hybridization identified fibrous cells, osteogenic cells, and microvascular wall cells as primary cellular sources of FGF-23 expression in FD tissue.
Serum FGF-23 concentrations were significantly elevated in FD/MAS patients compared to normal controls, with significantly higher levels in patients exhibiting renal phosphate wasting compared to those without.
Circulating FGF-23 levels correlated positively with total skeletal disease burden and bone turnover markers of disease activity.

Cite This Study

Riminucci et al. (2003) studied this question.

synapsesocial.com/papers/69daa4df00ab073a27838a43 https://doi.org/10.1172/jci18399

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