Osteoporosis: New Experimental Therapy for Bone Loss
In Germany, about six million people suffer from osteoporosis (bone loss). With the disease, the bone substance is broken down throughout the skeleton and the structure of the bones changes. Researchers are now reporting a new therapythe loss bone mass can restore.
Osteoporosis is a disease in which bones become porous and break easily. The disease is widespread. In Germany, at least six million people are living with the diagnosis, writes the German Rheumatism League on their website. Researchers now report in the journal “EMBO molecular medicine“about a new RNA technology against bone loss.
Affects more women than men
Like the University Hospital of Munich (LMU Klinikum) in a recent Message explained, osteoporosis is a bone disease, which affects no less than five million women and a good one million men in Germany alone – mainly in old age.
During the disease, bone mass decreases and bone strength decreases. The consequence is a higher risk of aching – and in old age – equally dangerous pain. broken boneseven with the smallest fillers that cannot harm healthy bones.
Two promising microRNAs identified
Bone, an amazingly dynamic tissue, is constantly breaking down and rebuilding itself. Get excited for it metabolism certain cells: osteoclasts act as wrecking balls and osteoblasts act as builders who create new things.
In a healthy metabolism, the two processes are in one balance, controlled by a fine network of signaling molecules produced according to the instructions of certain genes. The activity of these genes is ultimately also controlled by so-called micro-RNAs (miRNAs).
The disturbed bone metabolism of patients with osteoporosis, for example medication provided, which should push the constructive processes.
A team led by Prof. Dr. doctor Eric Hesse and Prof. Dr. Hanna Taipaleenmäki from the Institute of Musculoskeletal Medicine at the LMU Clinic first injected healthy mice, after which around the 20 micro RNA whose bones have been removed.
“Among these we have microRNAs 19a and 19b as special promising identified”, explain Professor Taipaleenmäki and Professor Hesse. These two microRNAs are hyperactive in the bones of patients with reduced bone mass and mice with impaired bone metabolism.
“This suggests that they bone metabolism can unbalance it”according to the researchers.
Disease-Related Bone Mass Loss Reversed
The scientists then created two so-called antisense miRNA molecules manufactured, which bind precisely to microRNAs 19a and 19b and thus deactivate their function.
This new therapy activates osteoblasts injected into mice with osteoporosis. In particular, however, overactive osteoclasts are inhibited. “We have seen that the loss of bone mass associated with the disease fact can be done”explain the researchers. “We’re essentially reversing the disease process.”
For the new treatment approach To further develop patients with impaired bone metabolism, the two experts founded a start-up. The technology is already patented. If all goes well, the new therapy could be tested on humans in a few years. (ad)
Author and source information
This text corresponds to the specifications of the specialized medical literature, medical guidelines and current studies and has been verified by health professionals.
Sources:
LMU Klinikum: New RNA technology against bone loss, (accessed on: October 10, 2022), LMU Clinic
Hanna Taipaleenmäki, Hiroaki Saito, Saskia Schröder, Miki Maeda, Ramona Mettler, Matthias Ring, Ewa Rollmann, Andreas Gasser, Carl Haasper, Thorsten Gehrke, Alexander Weiss, Steffen K. Grimm & Eric Hesse: Antagonizing microRNA-19a/b increases the Anabolic PTH Action and Restore Bone Mass in Osteoporosis in Mice; in: EMBO Molecular Medicine, (published: 2022-10-04), EMBO molecular medicine
German Rheumatism League: Osteoporosis: causes, symptoms, therapy, (accessed: October 10, 2022), German Rheumatism League
Important Note: This article contains general advice only and should not be used for self-diagnosis or treatment. It cannot substitute a visit to the doctor.