Scientific Meeting Genootschap
On Monday 2 October 2017 you are welcome at the Scientific Meeting of the Genootschap. The theme of the meeting is “Oral ecology and inflammation-driven bone resorption”.
|Datum||2 oktober 2017|
|Tijd||18:00 – 20:00|
- Prof. Dr. E. (Egija) Zaura
““Dental plaque – a friend or a foe? The role of microbial symbionts on our wellbeing”“
- Dr. ir. T.J. (Teun) de Vries
“Osteoclasts and inflammation driven bone loss“
Programme and location
You are welcome from 17.30h for coffee, tea, and sandwiches. The lectures will start at 18.00h and end around 19.30h. After the lectures drinks will be served.
The location is room Lecture room 0Z40, ACTA, Gustav Mahlerlaan 3004, 1081 LA Amsterdam.
The meeting is open for members of the Genootschap, employees and PhD-students from AMC, FNWI, and ACTA of the University of Amsterdam and employees and PhD-students from FALW, FEW and VUMC of the Free University Amsterdam.
We would like to ask you to register for this meeting via email@example.com.
Osteoclasts and inflammation driven bone loss
dr. Teun J. de Vries
Organ-specific specialization of macrophages has been acknowledged many decades ago. Heterogeneity of osteoclasts, the multinucleated bone resorbing cells that arise through fusion of monocyte/macrophage precursors, however, is a relatively new concept. Each skeletal site may have its own unique type of osteoclast. One way to explain the skeletal site heterogeneity of osteoclasts, is to assume that different precursor cells exist that respond uniquely to osteoclast differentiation stimuli. The concept of osteoclast heterogeneity is an attractive concept for specific interference of osteoclasts that are formed during inflammation, such as is the case of periodontitis and rheumatoid arthritis. We recently identified three mouse bone marrow precursors that differentiate at different pace. Besides this, they also respond differently to growth factor macrophage colony stimulating factor (M-CSF) and inflammatory cytokines interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α). Two prime findings that are important for understanding flexibility of osteoclast differentiation in the context of inflammation will be highlighted. First of all, life span of osteoclasts derived from these three precursor types may differ dramatically. IL-1β susceptible, large and short lived osteoclasts were identified as well as IL-1β insensitive, long lived osteoclasts. Secondly, two of our studies have identified conditions (either with M-CSF or with TNF-α ) and cell types that may evoke osteoclastogenesis insensitivity, making these precursor cells not able to respond to osteoclast differentiation factors. This could be the mechanism by which precursor cell make fate decisions, by either choosing macrophage ore osteoclast differentiation within the tissue. Adhesion to bone surpasses any osteoclastogenesis insensitivity, showing that osteoclasts’ local environment may unwrap physiologically important osteoclastogenesis insensitivity. Each skeletal site may do this in its own characteristic way.