Searchable abstracts of presentations at key conferences in endocrinology

ea0011oc55 | Calcium and bone OC49 Novartis Oncology Young Investigator Award | ECE2006

Thyroid hormones stimulate osteoblast differentiation but inhibit mineralization of bone nodules in vitro

Williams AJ , Barnard JC , Bassett JHD , Williams GR

Thyroid hormones stimulate bone formation and linear growth in children. Paradoxically, childhood thyrotoxicosis causes short stature and craniosynostosis due to early closure of the growth plates and skull sutures. In adults, however, thyroid hormone excess increases bone turnover and results in progressive bone loss and osteoporosis. Activating mutations of fibroblast growth factor receptor-3 (FGFR3) cause achondroplastic dwarfism and we have shown that T3 augments FGFR sign...

ea0011oc51 | Calcium and bone OC49 Novartis Oncology Young Investigator Award | ECE2006

TSH receptor action in osteoblasts and osteoclasts in vitro

Murphy E , Williams AJ , Galliford TM , Costagliola S , Vassart G , Bassett JHD , Williams GR

Recent studies suggest TSH inhibits bone remodeling, indicating that TSH deficiency rather than thyroid hormone excess could cause bone loss in thyrotoxicosis. The findings predict that TSH receptor (TSHR) stimulating antibodies (TSHRAb) should inhibit bone turnover, whereas Graves’ disease patients exhibit high bone turnover with increased fracture susceptibility. We characterized TSH-action in primary human and mouse osteoblasts and osteoclasts, and explored whether a p...

ea0011oc50 | Calcium and bone OC49 Novartis Oncology Young Investigator Award | ECE2006

Congenitally hypothyroid mice with (Pax8−/−) or without (hyt/hyt) functional TSH receptors (TSHR) display equivalent skeletal phenotypes

Williams GR , Swinhoe R , Murphy E , Williams AJ , Costagliola S , Vassart G , Howell PGT , Boyde A , Flamant F , Samarut J , Weiss R , Refetoff S , Bassett JHD

Studies of TSHR−/− mice suggest that TSH inhibits bone turnover, but these mice have congenital hypothyroidism and the actions of TSH cannot be separated from effects of thyroid hormone deficiency. We characterised skeletal development in hyt/hyt mice, which have a point mutation in the Tshr gene, and Pax8−/− mice with thyroid gland agenesis. Hyt/hyt mice have a 100-fold increase in TSH but inactive TSHRs, whereas Pax8&...