Searchable abstracts of presentations at key conferences on calcified tissues

ba0001pp147 | Cancer and bone: basic, translational and clinical | ECTS2013

Involvement of the co-receptor RAMP2 in the progression of breast cancer-induced osteolytic lesions

Cappariello Alfredo , Rucci Nadia , Capulli Mattia , Muraca Maurizio , Teti Anna

Bone is the primary site of metastasis for breast cancer, which leads mainly to osteolytic lesions, Cancer cells can expand into the bone for their ability to ‘dialogue’ with resident cells, interfering with the physiological processes of bone turnover. In this study, a large-scale analysis comparing gene expression of biopsies of bone and visceral metastases from human breast cancer patients showed that the receptor (G protein-coupled) activity modifying protein-2 (...

ba0002p68 | (1) | ICCBH2013

Engineered tridimensional hydroxyapatite scaffold to support bone resorption

Cappariello Alfredo , Mirabile Eleonora , Muraca Maurizio , Teti Anna

Objective: In many traumatic or pathological conditions, bone turnover is low and osteoclast activity is reduced or abolished. We developed innovative hydroxyapatite (HA) scaffolds carrying RANKL expressing cells with the aim of supporting bone resorption when this is defective. Membrane-bound (m)RANKL is cleaved into soluble (s)RANKL by MMP14. We hypothesized that the osteoclastogenic potential of RANKL-producing cells could be improved if they were seeded on scaffolds engine...

ba0003pp405 | Other diseases of bone and mineral metabolism | ECTS2014

Innovative cell-based strategy for systemic delivery of soluble RANKL in RANKL-deficient osteopetrotic mice

Cappariello Alfredo , Paone Riccardo , Capulli Mattia , Rucci Nadia , Muraca Maurizio , Teti Anna

In autosomal recessive osteopetrosis due to mutations of the TNFSF11 gene, deficiency of the pro-osteoclastogenic cytokine RANKL prevents osteoclast formation. RANKL is a membrane-bound protein cleaved into active soluble (s)RANKL by various enzymes, including metalloproteinase 14 (MMP14). We created a bio-device that released sRANKL and induced osteoclastogenesis in tnfsf11−/− mice. We tested various RANKL cell sources, and used mouse primary calvarial osteoblasts...