The US National Institutes of Health (NIH) has reported that denosumab significantly reduced abnormal bone turnover in fibrous dysplasia adult patients in a clinical trial.
Bone turnover is a process where old bone is replaced with new bone continuously. It is unusually accelerated in fibrous dysplasia and contributes to bone abnormalities.
The Phase II clinical trial was conducted by researchers from the NIH Clinical Center and the National Institute of Dental and Craniofacial Research (NIDCR) in eight women, who received high denosumab doses for six months.
Published in the New England Journal of Medicine, the findings demonstrated that denosumab might improve quality of life of patients by enabling healthy formation of bone.
The scans and bone biopsies of the participants demonstrated reduction in bone turnover in lesions, at the end of the treatment period.
According to the findings, proteins in the blood that are associated with bone turnover dropped to normal levels, and patients had reduction in complications while receiving treatment with denosumab.
How well do you really know your competitors?
Access the most comprehensive Company Profiles on the market, powered by GlobalData. Save hours of research. Gain competitive edge.
Your download email will arrive shortly
Not ready to buy yet? Download a free sample
We are confident about the unique quality of our Company Profiles. However, we want you to make the most beneficial decision for your business, so we offer a free sample that you can download by submitting the below formBy GlobalData
NIDCR clinical investigator Alison Boyce said: “Surgery is still the standard treatment for fractures and deformities caused by fibrous dysplasia.
“Denosumab is the first medication that appears to affect how fibrous dysplasia lesions behave and improves patients’ disease outcomes.”
The US Food and Drug Administration licensed denosumab for the treatment of bone problems caused from osteoporosis and cancer.
The medication works by blocking receptor activator of nuclear factor kappa-Β ligand (RANKL) protein that is elevated in fibrous dysplasia patients.