Bone Lab Dresden
Maintaining lifelong bone health remains a challenge. Therefore, our team works on several research projects linking bone research with diabetes, hematology, immunology, endocrinology, oncology, and materials science. Through our research, we expect to translate bone discoveries into more effective therapies for patients.
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Meet us at ECTS!
Every year about 1,000 basic scientists and clinical researchers from 55 countries come together at the ECTS to review and discuss latest advances in the musculoskeletal field
A special highlight this year will be the 50th year anniversary of bisphosphonates. Everyone in the field knows their history and impact on clinical medicine, but what will be their future? A forward looking session will review future developments. Also new this year, the meeting will include relevant hot clinical sessions to help managing patients going along the newest knowledge in the field.
The Bone Lab holds several talks and leads academy chairs. Come and join us:
Ulrike Baschant: The iron-sensing receptor #Tfr2 regulates #osteoclastogenesis and the #differentiation ability of hematopoietic stem cells; PLO06, Plenary Oral Presentations 1: Rare Musculoskeletal Diseases; Room: Pàtria, Sunday 12.05, 17:20-17:27
Martina Rauner: Novel mechanistic aspects and treatment of fibrodysplasia ossificans progressiva (#FOP), @Martina_MR7; WG6: Rare Bone Diseases, Rare Disorders with Increased/Ectopic Bone Formation Liszt 3, Friday 10.05, 18:00-18:30
Heike Weidner: Acvr2b ligand trap (luspatercept) improves bone mass in myelodysplastic mice and mice with ovariectomy-induced bone loss; Room: Bartók, Tuesday 14.05, 9:45-9:52
Elena Tsourdi: Next generation synergy session: Most exciting developments in the musculoskeletal field; Room Lehár 1+2, Friday 10.05 at 18:45
Stefanie Thiele: Chronic inﬂammation in HLA-B27 transgenic rats, a model of spondyloarthritis, results in body and bone marrow fat depletion; Room Lehár 1+2, Monday 13.05, 19:00-19:06
Franziska Lademann: Thyroid hormones augment osteoblast differentiation via the BMP-Smad1/5 signaling pathway; Room: Bartók, Monday 13.05, 9:45-9:52
Paula Goes: Loss of Dkk-1 in osteocytes prevents alveolar bone loss in mice subjected to experimental periodontitis; Room: Pàtria, Tuesday 14.05, 12:45-12:52
Maria G. Ledesma-Colunga: Hepcidin-resistant ferroportin mutation causes low bone mass in mice; Room: Bartók, Monday 13.05, 10:10-10:30
Andy Göbel: Potentiated anti-tumor effects in human osteotropic breast cancer cells by combined inhibition of the mevalonate pathway and the p38 kinase; P064, Poster loft
And vote for us and our science sketches:
Juliane Colditz https://youtu.be/7tD9hZTdRjU Facebook: https://www.facebook.com/644035099132136/posts/1109254232610218?s=1384931011
Franziska Lademann’s “MCT8 in Bone“: https://youtu.be/hNDDeCHRoD0 Facebook: https://www.facebook.com/644035099132136/posts/1109254992610142?s=1384931011
Franziska Lademann wins this year’s Von Recklinghausen Prize
The German Society for Endocrinology (DGE) supports and awards outstanding achievements in basic and clinical research . The Von Recklinghausen Award honors outstanding original scientific work in the field of calcium regulating hormones and bone metabolism. Franziska Lademann won this year’s award with her work on “Lack of the thyroid hormone transporter MCT8 in osteoblast and osteoclast progenitors increases trabecular bone in male mice”! Thyroid hormones are important for maintaining a healthy bone. Their transport into target cells is mediated by transporter proteins, such as the monocarboxylate transporter 8 (Mct8). Targeted knockdown of Mct8 gene expression in bone-building osteoblasts as well as bone-degrading osteoclasts in male mice led to an increase in trabecular bone mass. Both murine models suggest that MCT8 plays an important role in bone metabolism. Further experiments are needed to reveal the exact cellular mechanisms and processes behind it. The award ceremony took place at the annual conference of the German Society of Endocrinology on 21.03.2019 in Göttingen. Congratulations!
Just in time for the “Tag der Seltenen Erkrankungen” our researchers discover protein for more mobility
Only a few know the rare bone disease FOP: as in a nightmare, muscles and connective tissue are transformed into bone – and those affected are literally walled up alive. As a result, these patients become prisoners of their own body. Scientists of the Faculty of Medicine Carl Gustav Carus at the TU Dresden have now discovered a protein that inhibits excessive bone formation in FOP. In the future, this could be a therapeutic approach. The discovery is patented and the results of the study were published in the journal “Nature Metabolism”.
A total of four million children and adults in Germany are affected by one of more than 6,000 rare diseases. Many of these diseases are still rather unexplored, and there is still no effective therapy for the majority of these diseases. Take Fibrodysplasia Ossificans Progressiva (FOP). For patients, the diagnosis means the progressive ossification of soft tissue and muscles. Healthy muscles, ligaments and tendons transform into bones – all in the wrong place – resulting in stiffness and permanent immobility as if you were permanently trapped in a cast. The growth of bone-like structures where usually no bone is (ectopic ossification) may occur without warning or is triggered by a slight bump. The underlying cause is a gene defect that leads to a defective building plan for the ACVR1 receptor.
Scientists of the Bone Lab of the University Hospital at the TU Dresden have now discovered a protein that links two apparently unrelated systems. Transferrin receptor-2 (Tfr2), responsible for iron metabolism, was discovered as a new component in bone metabolism. Tfr2 binds to so-called bone morphogenetic proteins (BMPs), which are responsible for the mineralization of bone. Together with an interdisciplinary team of international researchers, the Bone Lab has now discovered that the binding region of Tfr2 can also be used to neutralize BMPs to prevent misplaced bone formation. Professor Martina Rauner and her colleagues were surprised: “When we saw how potent the binding region of Tfr2 inhibited the undesired soft tissue ossification in the animal model, we realized that this discovery may have the potential for clinical development.” Martina Rauner, biotechnologist and scientific director of the “Bone Lab” has dedicated her career to the study of bone diseases. It took years of intensive collaboration to decipher the therapeutic potential.
So far, there is no suitable therapy for the approximately 700 patients worldwide and the 30 people affected by FOP in Germany. However, now there is new hope, states Dr Ulrike Baschant: “Kymab, a therapeutic antibody company in Cambridge, will promote the clinical development of Tfr2 based on our discovery in Dresden.” This landmark discovery is significant not only for patients with FOP, but also for those with more common skeletal disorders, such as heterotopic ossification, a disease that occurs after hip replacement surgery or major trauma. The two main authors, Martina Rauner and Ulrike Baschant, report about their finding in the journal Nature Metabolism. The discovery of the protein was the result of international cooperation for many years, amongst others with scientists from the University of Torino in Italy. With the help of a dozen scientists, they worked in the lab to solve another puzzle of science. Martina Rauner is happy that the “newly created knowledge may serve novel therapies that could improve the lives of children and adults with bone diseases”. Ulrike Baschant adds, “It is a decisive step towards regaining physical independence and personal freedom!”
Bone Lab Dresden
Medizinische Klinik und Poliklinik III
Universitätsklinikum Carl Gustav Carus Dresden
Phone: +49 (0)351 458-3173
Fetscherstraße 74 · 01307 Dresden · Germany