Osteoclast precursors in inflamed tissues.
I am born and raised in Gothenburg, Sweden. In the beginning of 2014 I finished my Master of Science in Biotechnology and Tissue Engineering at Chalmers University of Technology. The focus of my MSc thesis was on osteoblasts and the possibility to steer their production of osteoid by modifying the stiffness of the culturing substrate. I am since April 2014 enrolled in Euroclast as an Early Stage Researcher at Academic Centre for Dentistry Amsterdam (ACTA) in the Netherlands. My hobbies are reading, driving my motorbike and drawing. My email address is firstname.lastname@example.org
Teun de Vries
After my M.Sc. degree in (Cell) Biology from the Agricultural University of Wageningen, I spent eight years of research in melanoma progression at the Radboud University Nijmegen, The Netherlands. I started on osteoclastogenesis research in 1999 at the Department of Periodontology at the Academic Centre for Dentistry Amsterdam (ACTA). I am involved as PI and co-PI in both Euroclast projects run in Amsterdam. And when I am not in the lab…..I love to sing and am member of a choir. My email address is email@example.com
I am the coordinator of the Euroclast. In 1971 I started as an EM technician at the academic medical center in Amsterdam. I studied Biology at the University of Utrecht and obtained my PhD in 1987 at the University of Amsterdam. In 2003 I became professor of Oral Cell Biology and in 2006 I became director of research at the Academic Center for Dentistry Amsterdam (ACTA). Since November of this year I am officially retired but in December I got a part-time appointment at ACTA for the Euroclast project. In my spare time I love to travel to observe and photograph wildlife, especially birds. My email address is: firstname.lastname@example.org
This Euroclast project is focused upon the priming of osteoclast precursors and the influence of inflammatory factors, like interleukin-17, on this process. It is well known that blood contains different subsets of osteoclast precursors with distinct properties, but the capacity of these subsets to differentiate into osteoclasts and how inflammatory cytokines influence this differentiation is unknown.
The autoimmune skeletal disease, rheumatoid arthritis, results in severe bone destruction, mainly attributed to an abnormal activation of osteoclasts, and is estimated to affect 1% of the worldwide population. The severity of this disease is strongly correlated with high concentrations of circulating interleukin-17. We will examine how the different osteoclast subsets we have identified respond to IL-17 to try to correlate this with the presence of overactive osteoclasts in affected joints in rheumatoid arthritis.
Our postal address is:
Oral Cell Biology
Gustav Mahler Laan 3004
1081 LA AMSTERDAM
Say “cheese!” Me, Sara, with supervisors Teun and Vincent and fellow Euroclast ESR Yixuan