What’s new in Bone Research – anabolics, tissue repair, therapeutic strategies and more

Hatfield, Herts
Friday, 20 October 2006

What’s new in Bone Research – anabolics, tissue repair, therapeutic strategies and more
Friday, 20 October 2006 09:00 - 17:00 (GMT)

The Fielder Centre
Hatfield Business Park
Hatfield Avenue
AL10 9FL
United Kingdom

Map and Directions

One of the greatest challenges in bone research today is how to replace bone tissue once it is lost.  Many bone diseases including osteoporosis, arthritis, and periodontal disease, could all benefit from new therapeutic strategies. This meeting is designed to highlight the latest developments in anabolic bone agents and methods of tissue repair in bone. Dr Nikki Horwood - London (Meetings chair)

09:00 – 09:30 Registration – tea/coffee and biscuits

09:30 – 09:40 Introduction by the Chair - Dr. Nikki Horwood, Imperial College

09:40 – 10:10 Stem cell-based therapeutic strategies for skeletal repair: from bench to bedside Dr Cosimo De Bari - King's College London, UK
Mesenchymal 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.

10:10– 10:40 Thyroid hormone and the maintenance of the adult skeleton Dr Duncan Bassett - Imperial College, UK
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.

10:40 - 11:00 Mid-morning break: tea/coffee

11:00 –11:30 Bone fragility and its regulation by the osteocyte’s old anabolics Dr Jonathan Reeve - Addenbrooke’s Hospital Cambridge, UK
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.

11:30 – 12:00 Growth control and signalling pathways in osteoblast differentiation Dr Agamemnon Grigoriadis, King's College & Guy's Hospital London, UK

12:00 – 12:30 Importance of vesicular trafficking in bone formation Dr Gudrun Stenbeck - Bone and Mineral Centre, London, UK

12:30 - 13:15 Lunch

13:15 - 13:45 The effect of thalidomide and bortezomib on bone disease of multiple myeloma Dr Evangelos Terpos, Division of Investigative Science, Imperial College London, UK
Thalidomide and bortezomib have shown a considerable anti-myeloma effect. The aim of this talk is to summarize the available data for their effect on myeloma bone disease. Thalidomide produces a significant reduction of bone resorption through alterations in the RANKL/osteoprotegerin system, which is crucial for osteoclast activation. However, it has shown no effect on bone formation which remains suppressed. Bortezomib, which is a proteasome inhibitor, not only reduces bone resorption but also normalizes bone formation through the reduction of osteoblast inhibitors, such as dickkopf-1. More importantly, bortezomib effect on bones seems to be irrespective of response to therapy.Importance of vesicular trafficking in bone formation

13:45 - 14:15  Resorpable solutions for hard tissue replacement and fracture fixation? Professor Chris Rudd University of Nottingham, UK
Professor Rudd will describe recent developments at the University of Nottingham towards a fully resorpable composite for hard tissue replacement or fracture fixation. The talk will cover the development of materials, processes and properties of aliphatic polyesters reinforced with long fibres of phosphate glasses.

14:15 – 14:45 Bone Healing: The effect of non-steroidal anti-inflammatory agents on mesenchymal stem cell proliferation and differentiation Prof. Peter V. Giannoudis, Academic Department of Trauma and Orthopaedic Surgery, School of Medicine, University of Leeds, St James's University Hospital, UK.
Bone healing is initiated with the proliferation of progenitor cells followed by endochondral ossification. Several drugs especially Non Steroidal Anti-Inflammatory Drugs (NSAIDs) have been convicted to interfere with this process. The purpose of this study was to elucidate the direct effect of these drugs on bone healing and consequently on endochondral ossification. Cancellous bone samples were obtained intra-operatively from 10 consecutive adult patients suffering from lower extremity fractures requiring surgical intervention. There were 6 male and 4 female with a mean age of 43 (range 16 to 81). Mesenchymal Stem Cells (MSCs) were isolated by enzymatic digestion. Cells were cultured in standard tissue culture conditions and freely proliferated till passage (P2). Subsequently, cells were forced to differentiate towards chondrogenic lineage. The drugs Diclophenac and Ketorolac were added in the medium in concentrations similar to the level in human circulation after administration. Comparison was performed with control group of untreated cells. After three weeks (21 days) of culture the pellets was removed and their content on sulphated Glycosaminoglycans (sGAG) was measured. Prostaglandin E2 (PGE-2) was also measured throughout the course of differentiation. RT-PCR was performed on Cox-1 and Cox-2 expression of the untreated cell. Finally, the morphological appearance of the pellets was studied. The results revealed a decrease of sGAG content of pellets treated with Diclophenac and Ketorolac by 39 % and 51 % respectively was noted. Diclophenac seems to have a milder effect compared to Ketorolac. PGE-2 production was severely decreased (30 fold) in the pellets treated with both drugs compared with the untreated cells. RT-PCR revealed a thee-fold increase of Cox-2 expression during the first three days of chondrogenic differentiation and a gradual decrease over the following days. Cox-1 was low throughout the chondrogenic differentiation. The morphology of the treated chondrocytes and pellets’ size was altered. The above findings indicate that NSAIDS have a negative effect on the bone healing process especially on endochondral ossification. The pathway of this remains obscure but the decreased levels of PGE-2, in association of cellular determination to up-regulate Cox-2 expression and production of PGE-2 seems to be an important factor.

14:45 - 15:15 Title to be confirmed Mr John Hardy, Centre for Orthopaedic Biomechanics, University of Bath, UK

15:15 Chairan’s summing up

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