07:36am Wednesday 20 September 2017

Identifies mechanisms behind bone strength and fracture risk

Osteoporosis, or brittle bones, is a devastating age-related widespread disease. Around 25 percent of all who suffer a fractured hip after 80 years of age die within a year of the injury. At the same time, the causes behind the disease are largely unknown.

The medications against osteoporosis that are used today can effectively reduce the risk of fracture in the trabecular bone that is in the vertebra. But the medications are less efficient in reducing the risk of hip and forearm fractures, which are most dependent on cortical bone.

Regulation of bone strength

Researchers at the Sahlgrenska Academy at the University of Gothenburg have now discovered a new mechanism that highly contributes to the regulation of the cortical bone strength.

“We have identified a gene that codes for a protein, which in turn is produced by bone-forming cells in cortical bone. In our study, we show that the protein increases bone strength by inhibiting the formation of bone-degrading cells in cortical bone,” says Sofia Movérare-Skrtic, researcher at the Sahlgrenska Academy.

Reduce risk of fractures

“This new knowledge will be important in order for us to be able to reduce the risk of hip and forearm fractures in the long term,” says Claes Ohlsson, Professor at the Sahlgrenska Academy, who led the study:

“We hope that our results will lead to better possibilities of preventing and treating hip and forearm fractures, an area where there is currently a large medical need for new treatments.”

As early as two years ago, the Gothenburg researchers used genetic analyses of the genome to identify a gene that was strongly linked with forearm fractures. Now in the course of two years, they have mapped in detail the mechanisms behind this.

Translational approach

In recent years, the research world has identified genetic markers for several different diseases through extensive analyses of the genome, but in many cases, failed to identify the underlying mechanisms.

“We began with an unbiased genetic analysis, which was followed by the identification of a new pharmaceutical target through experimental studies. This translational approach, which is unique, has been very successful,” says Claes Ohlsson.

The article Osteoblast-derived WNT16 represses osteoclastogenesis and prevents cortical bone fragility fractures was published in Nature Medicine on October 12.

Link to journal

Contact:
Claes Ohlsson, Professor at the Center for Bone and Arthritis Research, the Sahlgrenska Academy at the University of Gothenburg
+46-70-683 2966
claes.ohlsson@medic.gu.se

 

BY: Krister Svahn
+4631786 38 69


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