- Hall A
- Click here for Hall B
08:30-10:00 |
SARCOPENIA: IMPACT OF NUTRITION ON MUSCLE MASS, STRENGTH AND PERFORFORMANCE IN OLDER ADULTS |
| Capsule |
Muscle strength plays an important role in determining risks for falls which result in fractures and other injuries. While bone loss has been recognized as an inevitable consequence of aging, sarcopenia – the gradual loss of skeletal muscle mass and strength that occurs with advancing age – has recently received increased attention. This session reviews the effect of nutrition on sarcopenia and muscle performance
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| Chairpersons | A.B. Maier, Netherlands C. Leeuwenburgh, USA |
| Muscle mass M. Vandewoude, Belgium |
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| Muscle performance M. Henriksen, Denmark |
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| Signaling pathway implicated in anabolic resistance: Effects of exercise and nutrition M. Francaux, Belgium |
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| Evaluation of the effects of nutritional supplements in the elderly population T. McAlindon, USA |
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| "Under 34" competition winner: Association between insulin resistance, muscle mass and muscle strength in proximal versus distal bodyparts in healthy young men T. Gysel, Belgium |
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| Objectives | To acquire knowledge of the following:
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10:30-12:00 |
LATEST UPDATES AND NEW TREATMENTS IN BMJD |
| Capsule | Bone cartilage and muscle undergo morphological and biochemical changes with aging that lead to degenerative lesions of these tissues. Some physiopathological pathways are common, indicating that some treatments could be effective on all of these tissues. This session is a general overview of the latest innovations in the management of patients with musculoskeletal disorders in elderly people in 2013 |
| Chairpersons | S. Toegel, Austria W. Zhang, UK |
| New therapeutics to manage sarcopenia in the elderly A.B. Maier, Netherlands |
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| Anabolic treatments and/or uncoupling of bone resorption and bone formation J.C. Gallagher, USA |
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| Chondroprotection in OA: Results of ERADIAS study P. Richette, France |
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| New non-pharmacological and pharmacological approaches to OA D. Hunter, Australia |
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| Objective | Upon completion of this session, the audience will have learned about recent advances in the treatment of osteoporosis, osteoarthritis and sarcopenia |
12:50-14:20 |
CARTILAGE HOMEOSTASIS AND DEGENERATION |
| Capsule |
Cartilage degradation is a key feature in OA. To better understand the mechanisms leading to an imbalance between catabolism and anabolism remains a challenge for scientists. Recently, researchers paid a particular attention for chondrocyte hypertrophic differentiation, angiogenesis or autophagy. These processes are directly linked to cartilage structural changes and could lead to the discovery of new therapeutic targets. This session overviews the recent advances in the understanding of cartilage degradation in OA
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| Chairpersons | S. Oesser, Germany M. Lotz, USA |
| Cell-matrix interface in cartilage homeostasis M. Cucchiarini, Germany |
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| Molecular mechanisms in cartilage remodelling and degeneration T. Pap, Germany |
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| Chondrocyte hypertrophic differentiation: Link to matrix angiogenesis and mineralization H. Kawaguchi, Japan |
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| Objectives | Upon completion of this session, the audience will have learned how to better understand the recent advance in OA pathophysiology |
14:40-16:10 |
INNOVATIONS IN SURGERY TO REPAIR MUSCULOSKELETAL TISSUESupported by an unrestricted grant from Synolyne S.A. |
| Capsule |
Musculoskeletal tissues regeneration is limited and associated with major complications. New approaches have been developed to promote tissue healing including, tissue engineering, cell therapy or growth factors delivery systems or platelet rich plasma injection. Some of these modalities are used in daily practice in sport and regenerative medicine, despite the absence of evidence based guidelines
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| Chairpersons | M. Balligand, Belgium P. Gillet, Belgium |
| Cartilage repair M. Brittberg, Sweden |
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| Subchondral bone repair H. Madry, Germany |
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| Tendon and muscle repair M. Brittberg, Sweden |
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| Objectives | Upon completion of this session, the audience will have learned to have a critical view of the recent advance in connective tissue repair |
16:30-18:00 |
MANAGING BONES IN PATIENTS WITH CANCER AND LIVER DISEASES |
| Capsule |
Bone metastasis is a common problem with poor specific treatments. However, can symptoms be alleviated to provide a better quality of life?
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| Chairpersons | M. Cohen-Solal, France P. Selby, UK |
| Bone metastasis and OP drugs | |
| Osteoporosis prevention after breast cancer S. Rozenberg, Belgium and C. Antoine, Belgium |
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| Osteoporosis in liver diseases N. Guanabens, Spain |
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| "Under 34" competition winner: Protective effect of a new chitosan biomaterial against the development of experimental osteoarthritis lesions in rabbits F. Oprenyeszk, Belgium |
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| Objectives | To acquire knowledge of the following:
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- Hall B
- Click here for Hall A
08:30-10:00 |
BIOMARKERS TO PREDICT OA PROGRESSIONSupported by an unrestricted grant from Artialis |
| Capsule |
Wet biomarkers include gene and protein derived markers such DNA, RNA, protein epitopes or post-translational modified epitope. One important challenge for these biomarkers is the prediction of OA onset and progression. Some of them are able to distinguish radiological progressors and non-progressors. These tools could be used in a personalized approach to OA patients and to select patients for clinical trials
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| Chairpersons | J. Loughlin, UK J.A. Roman-Blas, Peru |
| Mitochondrial gene polymorphisms relating to OA F.J. Blanco, Spain |
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| Protein biomarkers to identify OA progressors Y. Henrotin, Belgium |
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| Imaging markers to predict OA progression D. Hunter, Australia |
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| "Under 34" competition winner: Disability and not osteoarthritis predicts cardiovascular disease. A population-based cohort study T. Hoeven, Netherlands |
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| Objective | Upon completion of this session, the audience will have learned to take note of the latest advances in the field of OA biomarkers |
10:30-12:00 |
OSTEOARTHRITIS AND THE FUTURE OF THERAPY: SHOULD WE INVEST IN BASIC RESEARCH OR IN CLINICAL CARE PROGRAMS ? |
| Capsule | Despite the progress in our understanding of the molecular and cellular biology of cartilage and bone, until now the search for disease modifying or chondroprotective drugs has been frustrating. Recent genetic studies have highlighted additional difficulties associated with patient-beneficial progress , for instance the heterogeneity of the disease phenotypes. When taking into account the overall impact of the disease in an aging population, many voices suggest to privelege clinical care over drug development programs. Is this the right choice? This session will foster the debate |
| Chairpersons | R. Lories, Belgium T. Pap, Germany |
| Functional genomics J. Loughlin, UK |
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| Phenotyping in OA: Connecting basic science with clinical practice J.W.J. Bijlsma, Netherlands |
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| Natural antioxidants to treat inflammatory joint diseases? H.K. Biesalski, Germany |
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| Objectives | Upon completion of this session, the audience will have learned: |
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12:50-14:20 |
IS THERE A BETTER TREATMENT THAN PLACEBO FOR OA? |
| Capsule |
In OA clinical trials, 50 to 60% of patients respond to placebo. Further, the effective size of treatments are globally modest. In parallel, drugs like NSAIDs which are largely used in OA are associated with severe adverse effects limiting their use in elderly people. Therefore, before using these drugs the benefit/risk ratio should be considered. An alternative would be the administration of placebo. Is this realistic and ethically acceptable? This session will try to answer at these questions
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| Chairpersons | D. Hunter, Australia F.J. Blanco, Spain |
Debate: Is there a consensus on whether the practitioner should be encouraged to use placebos for OA?Clinician point of viewP. Dieppe, UK Methodologist point of view W. Zhang, UK Discussion |
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| Can we limit the impact of placebo effect in randomized clinical trials? M. Marty, France |
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| Objectives | Upon completion of this session, the audience will have learned:
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14:40-16:10 |
NEW MOLECULES IN DEVELOPMENT |
| Capsule |
Activated immune cells infiltrate the joint in RA and produce cytokines and chemokines. These proteins bind to cells surface receptors, initiating signal transduction cascade through intracellular signaling pathways. These cells cause inflammation and joint destruction. New developments in small molecules can control the task and have been found to have a good profile regarding efficacy and safety
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| Chairpersons | R. Handa, India O. Gualillo, Spain |
| Development of JAK inhibitors for RA T. Hendrikx, Netherlands |
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| When to use them P. Durez, Belgium |
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| Are they all similar in pharmacokinetic, efficacy and safety? S. Gay, Switzerland |
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| Objectives | Upon completion of this session, the audience will have learned:
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16:30-18:00 |
STRATEGIES IN EARLY RA AND SPONDYLOARTHROPATHIES |
| Capsule |
Different lines of evidence suggest that current biological therapies directed at different molecules or cells have similar efficacy in RA, and target similar populations of patients. Distinct biological effects of targeted therapies may not account for differences in response, but clinical desease activity assessment and targeting remission or low desease activity remain the most important tasks in clinical practice. New strategies being proposed are always interesting to study, especially in early RA
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| Chairpersons | A. Doria, Italy |
| Recent advances in pathogenic mechanisms in early RA A.I. Catrina, Sweden |
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| Early RA: Induction, treatment withdrawal and treat-to-target M. Scarpellini, Italy |
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Early diagnosis and early treatment: A new challenge in spondyloarthritis? |
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| Objectives | Upon completion of the session, the audience will have learned:
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