ICCBH2013 Oral Posters (1) (15 abstracts)
High FSH serum levels may support the altered bone remodeling in Turner syndrome patients
Giacomina Brunetti 1 , Anna Maria Ventura 2 , Laura Piacente 2 , Angela Oranger 1 , Maria Ciccarelli 2 , Giorgio Mori 3 , Silvia Colucci 1 , Luciano Cavallo 2 , Maria Grano 1 & Maria Felicia Faienza 2
1Section of Human Anatomy and Histology, Department of Basic Medical Sciences, Neuroscience and Sense Organs, University of Bari, Bari, Italy; 2Department of Biomedical Sciences and Human Oncology, University of Bari, Bari, Italy; 3Department of Biomedical Science, University of Foggia, Foggia, Italy.
Objective: Turner syndrome (TS) is a chromosomal aberration characterized by total or partial loss of one of the two X-chromosomes, and affects about 1 in every 2500 girls. TS patients can develop the bone disease with decreased bone density and selective reduction in cortical bone thickness, which probably contributes to the increased fracture risk. However, the mechanisms underlying the bone disease remain poorly understood. Thus, the aim of this study was to investigate the osteoclastogenic potential of unfractionated peripheral blood mononuclear cells (PBMCs) and T cell-depleted PBMC cultures from TS patients (mean age 10.44±3.48) with high or normal FSH serum level and controls.
Methods: PBMCs and T-cell depleted culture from patients and controls were cultured in presence/absence of M-CSF and RANKL, or neutralizing antibodies anti-RANKL and anti-TNF-α. At the end of the culture period, mature multinucleated OCs were identified as TRAP+ cells. By real-time PCR we studied gene expression in freshly isolated T cells and monocytes. ELISA were performed in sera and media.
Results: Spontaneous formation of active resorbing osteoclasts, without adding M-CSF and RANKL, occurred in PBMC cultures from TS patients with elevated FSH serum levels. Conversely, M-CSF and RANKL were essential to trigger and sustain osteoclastogenesis in PBMCs from controls as well as TS patients with normal FSH serum levels. T-cell depleted PBMC cultures from TS patients with high FSH serum level showed only a partial reduction of spontaneous osteoclast formation, suggesting that both monocytes and T cells have an important role supporting the elevated osteoclastogenesis. In fact, in these patients, the percentage of circulating osteoclast precursors (OCPs) is increased and monocytes expressed elevated c-fms, IL-1, TNF-α and RANK levels, whereas T cells showed high RANKL amounts. Moreover, elevated amount of RANKL were detected in PBMC culture media and sera from TS patients with high FSH circulating levels by ELISA. Finally, functional anti-RANKL and anti-TNF-α antibodies significantly inhibited osteoclastogenesis.
Conclusion: We showed for the first time the high osteoclastogenic potential of PBMCs from young TS patients with high FSH circulating levels. This condition could contribute to the bone disease that become evident in their adult life.
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Bone Abstracts
ISSN 2052-1219 (online)
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