The discovery of a key protein that blocks the activity of bone-forming cells could pave the way for new osteoporosis treatments, according to scientists.

More than 3.5 million people are thought to live with the condition, which weakens bones and makes them more likely to break.

Cells called osteoblasts that form bone tissue are transported to sites where new bone is needed by endothelial cells that line the inside of blood vessels.

But a study found that the presence of a protein, CLEC14A, on the outside of endothelial cells can stop the osteoblasts maturing to the point where they can form bone tissue.

Dr Amy Naylor, of the University of Birmingham, said: “In the experiments we performed, when CLEC14A protein is present the osteoblasts that were sharing a ride on the endothelial cells produce less bone.

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“Conversely, when the protein is removed, they produce more bone. 

“This additional understanding of how blood vessel cells control bone-forming osteoblasts under normal, healthy conditions provides an avenue to develop treatments for patients who have insufficient bone formation, for example in patients with fractures that do not heal, osteoporosis or with chronic inflammatory diseases.”

The breakthrough follows the success of the Sunday Express Better Bones campaign, which led to a Government commitment to end a postcode lottery for access to vital fracture liaison services.

Researchers studied osteoblast cells taken from two groups of mice, only one of which had been bred to produce the CLEC14A protein.

In lab tests, cells taken from the protein-free mice matured within four days, while those from mice producing CLEC14A matured eight days later.

The protein-free samples also saw a significant increase in mineralised bone tissue after 18 days.

Lucy Donaldson, director for research and health intelligence at Versus Arthritis, said: “We know that poor bone formation is an important driver of bone damage in osteoporosis and autoimmune inflammatory arthritis. 

“This can lead to disability, pain, and fatigue which impacts people’s lives in many ways, including their ability to work, the time they spend with family and friends, and their wellbeing.

“We’re proud to have funded Dr Naylor’s research which has improved our understanding of bone formation and remodelling. 

“We hope these findings will eventually lead to new treatment approaches for people with musculoskeletal conditions.”

Ms Donaldson added: “Whilst these findings are promising, we won’t rest until everyone with arthritis has access to treatments and interventions that let them live the lives they choose.”

The findings were published in the journal Communications Biology.

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