An international team has discovered a treatment against osteoporosis for postmenopausal women. This bone fragility affects 450,000 people over the age of 50 in Switzerland and is responsible for 75,000 fractures each year.
To achieve this treatment, which was published in the New England Journal of Medicine, researchers, including Serge Ferrari from Geneva, are interested in a protein that inhibits bone formation.
“It is an experience of nature that has put us on this track with people who are ‘fortunate’ to have a skeleton too massive,” explains the head of the department of bone diseases at the University Hospitals of Geneva (HUG) and professor at the Faculty of Medicine of the University of Geneva. “It gave us something to think about: there had to be a mutation in them that put them in advantage.”
Stopping the growth of the skeleton
A protein, sclerostin, is at the origin of this mutation. “This is what nature has invented to curb the growth of our skeleton and precisely in those families that have skeletons too big, this protein is mutated and is no longer functional. It allows the skeleton to grow a little immoderately, It has become a therapeutic target.”
Serge Ferrari recalls that the best way to inhibit a protein is to develop an antibody “that once injected, will cling to this protein and eliminate it from the body, freeing bone formation”. The treatment – which should be directed to severe cases of the disease – is thus administered once a month by intravenous.
“We were surprised to see that in addition to inhibiting this protein, the antibody decreased bone loss. We have a dual anti-resorbing and bone building action.”
The results of the first year of tests showed a reduction in the risk of vertebral fractures of nearly 75% and the risk of clinical fractures of 36%, reports the specialist of bone diseases. “Very encouraging results, because very fast.”