Searchable abstracts of presentations at key conferences on calcified tissues

ba0003pp392 | Other diseases of bone and mineral metabolism | ECTS2014

Serum concentration of bone tissue metabolism markers in 28 and 180-day-old Polish Large White pigs

Beveridge Louise , Struthers Allan , Khan Faisel , Jorde Rolf , Scragg Robert , MacDonald Helen , Witham Miles

Evaluation of time-related changes of serum biochemical bone metabolism markers was performed in male pigs. Control group (n=7) received saline. NanoCa group (n=7) received nanopartical calcium per os (Ace Nano Calcium, NanoTechWorld, Korea). Dex group (n=7) received dexamethasone (1 mg/kg/48 hr i.m.). NanoCa/Dex group (n=6) received simultaneously nanopartical calcium and dexamethasone the same as the groups NanoCa and Dex...

ba0002p106 | (1) | ICCBH2013

Acquired hypophosphatemic rickets in a 13-year-old boy presenting with knee pain and valgus deformity

Bowden Sasigarn , Beebe Allan , Wildman Sally

Background: Hypophosphatemic rickets commonly presents in early childhood as inherited disorders. Acquired hypophosphatemic rickets or osteomalacia is a rare condition in children caused by paraneoplastic production of phosphaturic factor or FGF23 and is called tumor-induced rickets or osteomalacia. Localization of tumor is important as hypophosphatemic rickets completely resolves after resection of tumor.Presenting problem: We present a challenging case...

ba0002p26 | (1) | ICCBH2013

Improvement in genu valgus deformity in hypophosphatemic rickets due to primary de Toni-DebrDebré-Fanconi syndrome treated with phosphate, calcitriol and alkali therapy

Bowden Sasigarn , Patel Hiren , Beebe Allan , McBride Kim

Background: Primary de Toni-Debré-Fanconi syndrome is a metabolic disorder characterized by hypophosphatemic rickets or osteomalacia, renal tubular acidosis, renal glycosuria, generalized aminoaciduria. It is a non-FGF23-mediated hypophosphatemic disorder, with primary defect in proximal tubular dysfunction. The orthopaedic sequela of this rare disorder in the literature is scarce.Presenting problem: We present a clinical case of a 10-year-old femal...

ba0003pp135 | Cell biology: osteoblasts and bone formation | ECTS2014

High-resolution molecular validation of self-renewal and spontaneous differentiation in adipose-tissue derived human mesenchymal stem cells cultured in human platelet lysate

Dudakovic Amel , Camilleri Emily , Riester Scott , Westendorf Jennifer , Kakar Sanjeev , Dietz Allan , van Wijnen Andre

Improving the effectiveness of adipose-derived human mesenchymal stromal/stem cells (AMSCs) for skeletal therapies requires a detailed molecular characterization of mechanisms supporting cell proliferation and multi-potency of AMSCs. We compared gene expression data obtained by high-throughput RNA sequencing and RT-qPCR of actively proliferating and uninduced post-proliferative AMSCs with flow cytometry data for mesenchymal stem cell markers (e.g., CD44, CD73/NT5E, CD90/THY1 a...

ba0003pp149 | Cell biology: osteoblasts and bone formation | ECTS2014

Telomerase promotes osteoblast differentiation by modulating IGF-signaling pathway

Saeed Hamid , Qiu Weimin , Li Chen , Flyvbjerg Allan , Abdallah Basem , Kassem Moustapha

The molecular mechanisms underlying telomere shortening and telomerase deficiency contributing to defective age-related bone formation are poorly studied. We have previously demonstrated the role of telomerase re-activation in enhancing osteoblast differentiation of BMSCs in vitro and in vivo. Here, we investigated further the signaling pathways underlying the regulatory function of telomerase in osteogenesis. Comparative microarray analysis of telomerase-ove...

ba0003pp362 | Other diseases of bone and mineral metabolism | ECTS2014

Osteogenesis imperfecta in adults: a cross sectional trial

Hald Jannie Dahl , Folkestad Lars , Andersen Jane , Harslof Torben , Lund Allan , Jens-Erik Beck Jensen , Brixen Kim , Langdahl Bente

Osteogenesis imperfecta (OI) is a hereditary disease with a generalized involvement of the connective tissue caused by collagen type 1 mutations. The clinical appearance is broad with fractures as the key symptom. Only few genotype–phenotype correlations have been established. We aim to characterize the Danish OI population thoroughly including DXA and HRpQCT, anthropometry, patient history, and genetic background.This cross-sectional study includes...