Click here to find out more

Meeting Highlights

Stem cell-based therapeutic strategies for skeletal tissue repairDr Cosimo De Bari - King's College LondonMesenchymal stem cells (MSCs) can be extensively expanded in culture while maintaining their multilineage differentiation potential and therefore are attractive for a use in skeletal tissue engineering protocols.We have identified and characterized MSCs from the adult human synovial membrane (SM), an easily accessible and rapidly self-renewing tissue. SM-MSCs can differentiate at the single cell level to cartilage, bone, adipocytes, and skeletal muscle.We are currently investigating the niche(s) of MSCs within the synovial membrane in vivo and their contribution to joint tissue homeostasis and repair using animal models.

Too much bone and not enough.
Dr Ken  Poole, University of Cambridge
A key factor in the control of bone remodelling is parathyroid hormone (PTH), the principal regulator of calcium homeostasis. Elevated levels of PTH increase bone turnover, leading to either anabolic or catabolic effects on the skeleton, dependent on the pattern and duration of elevation. It was recently shown that down regulation of sclerostin (a newly discovered osteocyte signal) occurs in response to intermittent PTH. The usual function of osteocytic sclerostin signalling appears to be to inhibit bone formation by active osteoblasts at an appropriate stage, by binding LRP5 and consequently inhibiting Wnt signalling. This mechanism protects against the deleterious effects of too much bone formation, as observed in the disease sclerosteosis, where sclerostin is absent due to a non-functioning transcript. These findings have rekindled interest in the key role played by osteocytes and bone lining cells in co-ordinating anabolic activity at the bone surface. Enhancing bone's anabolic activity through inhibition of these mechanisms may provide new treatment options for osteoporosis.

Importance of vesicular trafficking in bone formation
Dr Gudrun Stenbeck - Bone and Mineral Centre, London


Bone fragility and its regulation by the osteocyte’s old anabolics

Dr Jonathan Reeve - Addenbrooke’s Hospital Cambridge

The osteocyte is the primary sensor in bone of mechanical loading. It functions as part of a sycitium of similar cells linked by dendritic connections to each other and to bone surface cells (osteoblasts and lining cells). This talk will describe how osteocytes regulate bone mass and bone strength through secreting signalling molecules such as sclerostin and by provoking osteoclastic resorption through their own apoptosis.

 
Growth control and signalling pathways in osteoblast differentiation
Dr Agamemnon Grigoriadis

Thyroid hormone and the maintenance of the adult skeleton

Dr. Duncan Bassett - Imperial College

Thyroid hormone is essential for the normal development of endochondral and intramembranous bone and plays an important role in the linear growth and maintenance of bone mass. Childhood hypothyroidism results in retardation of skeletal development and growth arrest, whereas T3 excess leads to accelerated growth and bone formation. In adult thyrotoxicosis, there is increased bone remodelling, characterized by an imbalance between bone resorption and formation, which results in net bone loss and an increased risk for osteoporotic fracture. I will discuss the implications of our skeletal analysis in a series of mice genetically modified for the thyroid hormone receptor.

 

New Anabolics in Bone Research