People with osteoporosis suffer faster fractures.
Read aloud Australian researchers have taken a significant step toward developing effective osteoporosis drugs. So far, it has been virtually impossible to specifically stimulate bone formation without equally stimulating bone resorption. A research focus is therefore on the separation of these two metabolic processes. The scientists succeeded in experiments with mice to find a key protein that regulates the bone up and down via two different receptors. After shutting down the receptor responsible for the degradation in some animals, their bones had a much higher density, report Natalie Sims from the University of Melbourne and her team. The human skeleton is in a state of permanent remodeling: osteoclasts are degrading bone, while osteoblasts are beginning to rebuild. So that the bones do not proliferate excessively, an increase in the building osteoblasts is always accompanied by a corresponding increase in bone-eating cells. However, it is precisely this close connection between the processes of breakdown and development that makes the treatment of osteoporosis so difficult. Bone density also decreases as a disease called bone loss, which increases the risk of bone fractures. To counteract this, a targeted bone structure would have to be operated, which, however, requires a decoupling of the two metabolic processes.

Current research is focused on a protein called sclerostin, which inhibits bone formation. The protein was first discovered in people with excessive bone growth: A defect in the SOST gene had prevented the formation of sclerostin. If it were possible to artificially suppress the formation of sclerostin, it would be necessary to increase bone formation without simultaneously producing counterproductive phagocytes.

The Australian scientists therefore investigated the influence of another protein called Oncostatin M (OSM) on sclerostin production. OSM is produced by both osteoclasts and osteoblasts. In experiments with mice, the researchers now found that it docks to two different receptors, one to the OSM receptor (OSMR), on the other hand, the Leukemia Inhibitory Factor receptor (LIFR). In conjunction with OSMR, OSM stimulates the production of bone gland cells. In combination with LIFR, OSM blocks sclerostin production and thus limits the number of osteoblasts. In mice, in which the receptor LIFR was artificially blocked, the number of osteoblasts and thus also the bone density increased significantly.

ddp / science.de? Mascha Schacht Natalie Sims (University of Melbourne) et al .: Journal of Clinical Investigation, doi: 10.1172 / JCI40568

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